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Hepatocellular carcinoma : a clinico pathological study.

Retrograde lymphatic spread definition in betting Deregulated expression of fibroblast growth factor receptors FGFRs and their ligands plays critical roles in tumorigenesis. In cell motility assays, hydrogen peroxide treated cells showed significantly high cell motile activity, compared with untreated cells. The newest member of the VEGF family. Mice with lymphatic endothelial cell-specific deficiency of epsin 1 and 2 had dilated lymphatic capillaries, abnormally high VEGFR 3 abundance in collecting lymphatics, immature lymphatic valves, and defective lymph drainage. The baseline DcR3 concentration showed a strong positive correlation with inflammatory markers including high-sensitivity C-reactive protein, IL-6, intercellular adhesion molecule-1 ICAM-1and vascular cell adhesion molecule-1 VCAM
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Eur J Obstet Gynecol ; : — Cell proliferation is increased in the endometrium of women with endometriosis. Fertil Steril ; 64 : — Eutopic and ectopic stromal cells from patients with endometriosis exhibit differential invasive, adhesive, and proliferative behavior. Fertil Steril ; : — L1 cell adhesion molecule L1CAM as a pathogenetic factor in endometriosis. Fibrinolytic factors in endometriotic tissue, endometrium, peritoneal fluid, and plasma from women with endometriosis and in endometrium and peritoneal fluid from healthy women.

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Proteomic identification of neurotrophins in the eutopic endometrium of women with endometriosis. Fertil Steril ; 98 : — High density of small nerve fibres in the functional layer of the endometrium in women with endometriosis. Hum Reprod ; 21 : — Semin Reprod Med ; 28 : 36 — Aromatase expression in endometriosis. J Clin Endocrinol Metab ; 81 : — Changes in the T-helper cytokine profile and in lymphocyte activation at the systemic and local levels in women with endometriosis.

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Microvasc Res ; 21 : — Lymphangiogensis of normal endometrium and endometrial adenocarcinoma. Uterine lymphatic and blood micro-vessels in women with endometriosis through the menstrual cycle. J Endometr ; 2 : — Methods of detection of lymphatics and their changes with oestrous cycle. Int Angiol ; 6 : — Ueki M. Histologic study of endometriosis and examination of lymphatic drainage in and from the uterus.

Am J Obstet Gynecol ; : — Netter FH. New York : Ciba Pharmaceutical Company ; Google Preview. Intraoperative lymphatic mapping techniques for endometrial cancer. Expert Rev ; 11 : 83 — Routes of lymphatic spread: a study of consecutive patients with endometrial cancer. Gynecol Oncol ; 81 : — Ellis H.

Anatomy of the uterus. Anaesth Intensive Care Med ; 9 : — Intraabdominal lymphatic mapping to direct selective pelvic and paraaortic lymphadenectomy in women with high-risk endometrial cancer: results of a pilot study. Gynecol Oncol ; 62 : — Histological characteristics of healthy animal peritoneum.

Acta Vet ; 56 : — Trans-lymphatic metastasis in peritoneal dissemination. J Gastrointest Dig Syst ; 12 : 1 — 6. Lymphatic drainage of the peritoneal space: a pattern dependent on bowel lymphatics. Ann Surg Oncol ; 14 : — Dysregulation of vascular endothelial growth factors and their neuropilin receptors in the eutopic endometrium of women with endometriosis.

Reprod Sci ; 20 : — Vascular endothelial growth factor A and C gene expression in endometriosis. Hum Pathol ; 35 : — A novel pilot study of endometrial stromal cells and immune cell populations in sentinel uterine-draining lymph nodes during the menstrual cycle and in endometriosis. Endometrial stromal cells and immune cell populations within lymph nodes in a nonhuman primate model of endometriosis.

Reprod Sci ; 18 : — Lymphangiogenesis in deep infiltrating endometriosis. Hum Reprod ; 10 : 1 — 8. Lymphatic vessels in peritoneal endometriotic lesions. J Endometr ; 3 : 59 — High lymph vessel density and expression of lymphatic growth factors in peritoneal endometriosis. Reprod Sci ; 19 : — Girling J , Rogers P. The endometrial lymphatic vasculature: function and dysfunction.

Endocr Metabol Disord ; 13 : — Lymphangiogenesis and cancer metastasis. Nat Rev Cancer ; 2 : — Exp Eye Res ; 83 : — Up-regulation of vascular endothelial growth factor-D expression in clear cell renal cell carcinoma by CD a critical role in cancer cell tumorigenesis.

J Immunol ; : — Eur J Cancer ; 45 : — Interleukin 1beta, interleukin-6, and tumor necrosis factor-alpha in endometriotic tissue and in endometrium. Fertil Steril ; 75 : — TNF system in eutopic endometrium from women with endometriosis. Open J Obstet Gynecol ; 3 : — J Cell Biol ; : — Endometriosis-related endometrial dysfunctions. World Endometr Soc ; 8 : 7 — Insulin-like growth factors 1 and 2 induce lymphangiogenesis in vivo. Am J Reprod Immunol ; 37 : — The relationship between microvessel density, proliferative activity and expression of vascular endothelial growth factor-A and its receptors in eutopic endometrium and endometriotic lesions.

Reprod Res ; : — Expression of heparanase and angiopoietin-2 in patients with endometriosis. Angiopoietin-1, angiopoietin-2 and Tie-2 expression in eutopic endometrium in advanced endometriosis. Mol Hum Reprod ; 12 : — Immunoexpression of hepatocyte growth factor and c-Met receptor in the eutopic endometrium predicts the activity of ectopic endometrium.

Fertil Steril ; 79 : — Different basic fibroblast growth factor and fibroblast growth factor-antisense expression in eutopic endometrial stromal cells derived from women with and without endometriosis. J Clin Endocrinol Metab ; 88 : — Liao S , Padera TP. Lymphatic function and immune regulation in health and disease.

Lymphat Res Biol ; 11 : — Ivanov S , Martel C. Does lymphatic growth rely on immune cell function? OA Immunol ; 1 : 1 — 8. Berbic M , Fraser IS. Regulatory T cells and other leukocytes in the pathogenesis of endometriosis. J Reprod Immunol ; 88 : — Braun D , Dmowski P.

Endometriosis: abnormal endometrium and dysfunctional immune response. Curr Opin Obstet Gynecol ; 10 : — Dmowski P , Braun D. Immunology of endometriosis. Minerva Ginecol ; 18 : — Cavaillon JM. Cytokines and macrophages. Biomed Pharmacother ; 48 : — Cytokine secretion in macrophages and other cells: pathways and mediators.

Immunobiology ; : — Gong Y , Tempfer C. Regional lymphatic spread in women with pelvic endometriosis. Med Hypotheses ; 76 : — Metalloproteinases, vascular endothelial growth factor, and angiopoietin 1 and 2 in eutopic and ectopic endometrium. Fertil Steril ; 91 : — Chang Y , Ho Y.

Immunohistochemical analysis of insulin-like growth factor I, insulin-like growth factor I receptor and insulin-like growth factor II in endometriotic tissue and endometrium. Acta Obstet Gynecol Scand ; 76 : — Immunolocalization of angiopoietin 1 in human peritoneal endometriotic lesions. Transforming growth factor-beta 1 and insulin- like growth factor-1 expression in ovarian endometriotic cysts: a preliminary study.

Mol Med ; 7 : — Vascular density and distribution of vascular endothelial growth factor VEGF and its receptor VEGFR-2 Flk-1 are significantly higher in patients with deeply infiltrating endometriosis affecting the rectum. Fertil Steril ; 90 : — Insulin- like growth factor-1 isoform mRNA expression in women with endometriosis: eutopic endometrium versus endometriotic cyst. Mol Med ; 17 : 21 — Expression of vascular endothelial growth factor and thrombospondin-1 mRNA in patients with endometriosis.

Fertil Steril ; 78 : — Expressions of insulin-like growth factor I and its receptor in endometriosis. J Jilin Univ ; 33 : — Falcone B. Peritoneal fluid environment in endometriosis. Minerva Ginecol ; 55 : 1 — Am Soc Reprod Med ; 73 : — Pathogenesis of endometriosis: the role of peritoneal fluid. Gynecol Obstet Invest ; 47 : 23 — Vascular endothelial growth factor is produced by peritoneal fluid macrophages in endometriosis and is regulated by ovarian steroids.

J Clin Invest ; 98 : — Bedaiwy M , Falcone T. Peritoneal fluid environment in endometriosis: clinicopathological implications. Elevated levels of fibroblast growth factor-2 in serum from women with endometriosis. Chiang M , Hill J. Gynecol Obstet Invest ; 43 : — Phenotypic and functional studies of leukocytes in human endometrium and endometriosis.

Hum Reprod Update ; 4 : — Increased numbers of activated mast cells in endometriosis lesions positive for corticotropin-releasing hormone and urocorti. Am J Reprod Immunol ; 52 : — Immunohistochemical characterization of leucocyte subpopulations in endometriotic lesions. Arch Gynecol Obstet ; : — Potential involvement of the immune system in the development of endometriosis. Reprod Biol Endocrinol ; 1 : 1 — 9. Hum Reprod ; 28 : — The peritoneal environment in endometriosis.

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Endometriosis involving the ileocaecal junction with regional lymph node involvement in the baboon—striking pathological finding identical between the human and the baboon: a case report. Sheikh H. A year-old woman with a 7-month history of abdominal pain. Arch Pathol Lab Med ; : — Endometriosis and regional lymph node involvement in a rat model. Wien Klin Wochenschr ; : — Mouse model of surgically-induced endometriosis by auto-transplantation of uterine tissue.

J Exp Clin Cancer Res ; 29 : 1 — 9. A comparative study of the in vitro antioxidant activity of statins. Int J Cardiol ; 90 : — Could statins constitute a novel treatment for endometriosis? Systematic review of the literature. Angiogenesis and endometriosis. Obstet Gynecol Int ; : 1 — 8. Phenotype-based high-content chemical library screening identifies statins as inhibitors of in vivo lymphangiogenesis.

LYVE-1 immunohistochemical assessment of lymphangiogenesis in endometrial and lung cancer. J Clin Pathol ; 58 : — Red-Horse K. Lymphatic vessel dynamics in the uterine wall. Placenta ; 29 : 55 — Monoclonal antibody D, a new marker of lymphatic endothelium, reacts with Kaposi's sarcoma and a subset of angiosarcomas.

Mod Pathol ; 15 : — The use of LYVE-1 antibody for detecting lymphatic involvement in patients with malignant melanoma of known sentinel node status. Blocking neuropilin-2 function inhibits tumor cell metastasis. Cancer Cell ; 13 : — Tumor lymphangiogenesis as a potential therapeutic target. J Oncol ; : 1 — Wnt1 is anti-lymphangiogenic in a melanoma mouse model. J Invest Dermatol ; : — Tumor lymphatics. Semin Cancer Biol ; 19 : — From anti-angiogenesis to anti-lymphangiogenesis: emerging trends in cancer therapy.

Lymphat Res Biol ; 6 : — Incidence and risk of arm oedema following treatment for breast cancer: a three-year follow-up study. Vascular endothelial growth factor receptor-3 in lymphangiogenesis in wound healing. Am J Pathol ; : — Thiele W , Sleeman JP. Tumor-induced lymphangiogenesis: a target for cancer therapy? J Biotechnol ; : — Lymphedema: a comprehensive review. Ann Plast Surg ; 59 : — Blocking ephrinB2 with highly specific antibodies inhibits angiogenesis, lymphangiogenesis, and tumor growth.

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It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Medically Sound. Retrieved Andrews' Diseases of the Skin: clinical Dermatology. Saunders Elsevier. ICD - 10 : I Cardiovascular disease vessels. Arteritis Aortitis Buerger's disease. Carotid artery stenosis Renal artery stenosis.

Aortoiliac occlusive disease Degos disease Erythromelalgia Fibromuscular dysplasia Raynaud's phenomenon. Arteriovenous fistula Arteriovenous malformation Telangiectasia Hereditary hemorrhagic telangiectasia. Cherry hemangioma Halo nevus Spider angioma. Chronic venous insufficiency Chronic cerebrospinal venous insufficiency Superior vena cava syndrome Inferior vena cava syndrome Venous ulcer.

Hypertensive heart disease Hypertensive emergency Hypertensive nephropathy Essential hypertension Secondary hypertension Renovascular hypertension Benign hypertension Pulmonary hypertension Systolic hypertension White coat hypertension. Orthostatic hypotension. Lymphatic disease : organ and vessel diseases. Asplenia Asplenia with cardiovascular anomalies Accessory spleen Polysplenia Wandering spleen Splenomegaly Banti's syndrome Splenic infarction Splenic tumor.

Lymphadenopathy Generalized lymphadenopathy Castleman's disease Intranodal palisaded myofibroblastoma Kikuchi disease Tonsils see Template:Respiratory pathology. Lymphangitis Lymphangiectasia Lymphedema Primary lymphedema Congenital lymphedema Lymphedema praecox Lymphedema tarda Lymphedema—distichiasis syndrome Milroy's disease Secondary lymphedema Bullous lymphedema Factitial lymphedema Postinflammatory lymphedema Postmastectomy lymphangiosarcoma Waldmann disease.

Categories : Diseases of veins, lymphatic vessels and lymph nodes Lymphatic vessel diseases. Hidden categories: Webarchive template archiveis links. Namespaces Article Talk. Views Read Edit View history. Help Learn to edit Community portal Recent changes Upload file. Download as PDF Printable version. Wikimedia Commons. Inflamed lymph vessels [1]. Forearm lymphangitis due to cellulitis of the hand. Inflammation Arteritis Aortitis Buerger's disease.

Inflammation Phlebitis.

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Other nodes in lower neck, upper mediastina, and upper abdomen may have the same way. LNM is frequently present in the lower neck, upper mediastinum and perigastric area. It was found that the station of resected LN rather than the number of resected LN may be more important for lymphadenectomy. Other researches also had the same results. The lymphatic drainage of inner layer mucosa and submucosa and outer layer muscularispropria and adventitia of the esophagus is different.

The lymphatic metastasis seems to be in all the length of the esophagus for TEC. Therefore, 3FL with total esophagus resection or wide-range LN from neck to celiac area and total esophagus irradiation should be a radical method for TEC theoretically, even for an early-stage TEC. However, these methods result in more treatment intolerance and complications. Multimodality treatment has been widely investigated in order to improve the poor survival of EC.

However, we should balance the merits and faults of different therapies for making a standard treatment, not just put these therapies together. For a best multimodality treatment, it is questionable whether a standard lymphadenectomy is needed or whether LN irradiation with or without chemotherapy can be an effective alternative to lymphadenectomy, especially for LN in neck and upper mediastina where it is difficult for surgery. With the rapid development in different agencies, more safe and effective methods with a better quality of life are proposed for TEC.

Beyond that, the anatomical investigation of the lymphatic drainage of the esophagus is further needed. This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. Global cancer statistics, CA Cancer J Clin. Oesophageal cancer. Nat Rev Dis Primers. Results of a nationwide study on the three-field lymph node dissection of esophageal cancer. The overall prevalence of metastasis in T1 esophageal squamous cell carcinoma: a retrospective analysis of patients.

Ann Surg. Prognostic impact of upper, middle, and lower third mucosal or submucosal infiltration in early esophageal cancer. Prognostic significance of the size and number of lymph nodes on pre and post neoadjuvant chemotherapy CT in patients with pN0 esophageal squamous cell carcinoma: a 5-year follow-up study. Numeric pathologic lymph node classification shows prognostic superiority to topographic pN classification in esophageal squamous cell carcinoma.

Metastatic lymph node ratio demonstrates better prognostic stratification than pN staging in patients with esophageal squamous cell carcinoma after esophagectomy. Sci Rep. Assessment of lymph node ratio to replace the pN categories system of classification of the TNM system in esophageal squamous cell carcinoma. J Thorac Oncol. Three-field lymph node dissection in treating the esophageal cancer. J Thorac Dis. Clinical course and outcome after esophagectomy with three-field lymphadenectomy in esophageal cancer.

Langenbecks Arch Surg. Patterns of recurrence after oesophagectomy and postoperative chemoradiotherapy versus surgery alone for oesophageal squamous cell carcinoma. Br J Surg. The impact of histology on recurrence patterns in esophageal cancer treated with definitive chemoradiotherapy.

Radiother Oncol. Esophageal development and epithelial homeostasis. Anatomy and physiology of the thoracic lymphatic system. Thorac Surg Clin. Zhemchuzhnikova LE. Age changes in the anatomy of the lymphatic system of the human pancreas. Arkh Anat Gistol Embriol. J Clin Pathol. The esophageal wall. The normal configuration and interindividual differences in intramural lymphatic vessels of the esophagus.

J Thorac Cardiovasc Surg. Mucosal lymphatic vessels of the esophagus distant from the cancer margin: morphometrical analysis using 27 surgically removed specimens of squamous cell carcinoma located in the upper or middle thoracic esophagus. Okajimas Folia Anat Jpn. The organization of the lamina muscularis mucosae in the human esophagus. Arch Histol Cytol. The organization of the communication routes between the epithelium and lamina propria mucosae in the human esophagus. Esophageal carcinoma: depth of tumor invasion is predictive of regional lymph node status.

Ann Thorac Surg. Rice TW. Superficial oesophageal carcinoma: is there a need for three-field lymphadenectomy? Esophageal submucosa: the watershed for esophageal cancer. Lymphatic invasion according to D immunostaining is a strong predictor of nodal metastasis in superficial squamous cell carcinoma of the esophagus: algorithm for risk of nodal metastasis based on lymphatic invasion. Pathol Int. Retrograde lymphatic spread of esophageal cancer: a case report. Vascular and lymphatic properties of the superficial and deep lamina propria in Barrett esophagus.

Am J Surg Pathol. Anatomy of right recurrent nerve node: why does early metastasis of esophageal cancer occur in it? Surg Radiol Anat. Submucosal territory of the direct lymphatic drainage system to the thoracic duct in the human esophagus. Direct lymphatic drainage from the esophagus into the thoracic duct.

Last-intercalated node and direct lymphatic drainage into the thoracic duct from the thoracoabdominal viscera. Jpn J Thorac Cardiovasc Surg. Microscopic anatomy of the visceral fasciae. J Anat. A new concept of the anatomy of the thoracic oesophagus: the meso-oesophagus. Observational study during thoracoscopicesophagectomy.

Surg Endosc. Anatomy of the lymphatics. Surg Oncol Clin N Am. Extramural lymphatic drainage from the thoracic esophagus based on minute cadaveric dissections: fundamentals for the sentinel node navigation surgery for the thoracic esophageal cancers. Topographical anatomy of the bronchomediastinal lymph vessels: their relationships and formation of the collecting trunks.

Anat Sci Int. Riquet M. Bronchial arteries and lymphatics of the lung. Aikou T, Shimazu H. Difference in main lymphatic pathways from the lower esophagus and gastric cardia. Jpn J Surg. Natsugoe S. Experimental and clinical study on the lymphatic pathway draining from the distal esophagus and gastric cardia.

Nihon Geka Gakkai Zasshi. Pathomorphology of esophageal and gastric varices. Semin Liver Dis. Lymphatic drainage from esophagogastric tract: feasibility of endoscopic CT lymphography for direct visualization of pathways. Okanobu K. Microlymphatics and lymph flow. Physiol Rev. Thoracic duct tributaries from intrathoracic organs. Japan Esophageal Society.

Japanese classification of esophageal cancer, 11th edition: part I. Patterns of lymph node metastasis and survival for upper esophageal squamous cell carcinoma. Lymph node metastasis in thoracic esophageal carcinoma. J Surg Oncol. The pattern and prevalence of lymphatic spread in thoracic oesophageal squamous cell carcinoma. Eur J Cardiothorac Surg. Patterns of lymph node metastasis in 3-field dissection for carcinoma in the thoracic esophagus.

Surg Today. Patterns of lymphatic spread in thoracic esophageal cancer. Lymph node metastasis and recurrence in patients with a carcinoma of the thoracic esophagus who underwent three-field dissection. World J Surg. Evaluating the rational extent of dissection in radical esophagectomy for invasive carcinoma of the thoracic esophagus. Tachimori Y. Total mesoesophagealesophagectomy. Chin Med J.

A meta-analysis of lymph node metastasis rate for patients with thoracic oesophageal cancer and its implication in delineation of clinical target volume for radiation therapy. Br J Radiol. Therapeutic value of lymph node dissection for esophageal squamous cell carcinoma after neoadjuvant chemotherapy. J SurgOncol. Characteristics and clinical significance of lymph node metastases near the recurrent laryngeal nerve from thoracic esophageal carcinoma.

Genet Mol Res. Lymph node metastasis along the recurrent nerve chain is an indication for cervical lymph node dissection in thoracic esophageal cancer. Dis Esophagus. The prognostic relevance of subcarinal lymph node dissection in esophageal squamous cell carcinoma.

Ann Surg Oncol. Subcarinal node metastasis in thoracic esophageal squamous cell carcinoma. Unique distribution patterns of metastatic lymph nodes in patients with superficial carcinoma of the thoracic oesophagus. Cervical, mediastinal, and abdominal lymph node dissection three-field dissection for superficial carcinoma of the thoracic esophagus. Clinicopathologic analysis of lymph node metastasis in surgically resected superficial cancer of the thoracic esophagus.

Current trends in multimodality treatment of esophageal and gastroesophageal junction cancer — review article. Surg Oncol. This work is published and licensed by Dove Medical Press Limited. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.

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Advanced search. Home Journals Why publish with us? Keywords: esophageal carcinoma, lymphatic, lymph node metastasis,lymphadenectomy, radiotherapy Introduction Esophageal cancer EC is a common upper gastrointestinal tumor with a high incidence in Eastern Asia and Eastern and Southern Africa. Anatomy of lymphatic drainage Esophagus develops from the dorsal part of the foregut while the respiratory tract from the ventral part.

Normal intramural configurations The esophageal wall is composed of four layers: mucosa, submucosa, muscularis propria, and adventitia. Ejaculation is when semen comes out of your penis after reaching orgasm an intense feeling of pleasure. Retrograde ejaculation is when semen flows back into your bladder, instead of out through your penis.

When they reach the ejaculatory duct, the sperm mix with semen from the seminal vesicles and the prostate. During orgasm, your bladder neck closes and semen exits your body through your penis. When your bladder neck closes, it prevents semen from flowing back and going into your bladder. This means that semen flows backward into your bladder instead of forward through your penis.

RPLND is surgery to remove some of the lymph nodes in your abdomen belly. This surgery is a treatment for testicular cancer. During surgery, the nerves that control your bladder neck may be injured. Sometimes, these nerves can be spared, but it can take a month to several years for them to begin to work again.

Your doctor can tell you if surgery is an option for you. You may also get retrograde ejaculation after you have transurethral resection of the prostate TURP. TURP is a surgery done to treat urinary problems caused by an enlarged prostate. TURP may cause injury to the nerves causing your bladder neck to stay open during orgasm. Retrograde ejaculation can also be caused by diabetes, multiple sclerosis MS , certain medications, and spinal cord injury.

This is called a dry ejaculate. You will still be able to enjoy sexual activity. After sexual activity, your urine pee may be cloudy because it has semen in it. If you plan to have a family after your surgery, tell your doctor you want to bank your sperm before surgery.


Consequently, the defect in down-regulation of the highly activated receptors results in the increased signaling capacity from the intracellular compartments, and this may determine the severity of the diseases. Thomas, Susan N.

Lymphatic vessels transport interstitial fluid, soluble antigen, and immune cells from peripheral tissues to lymph nodes LNs , yet the contribution of peripheral lymphatic drainage to adaptive immunity remains poorly understood. We examined immune responses to dermal vaccination and contact hypersensitivity CHS challenge in K VEGFR - 3 -Ig mice, which lack dermal lymphatic capillaries and experience markedly depressed transport of solutes and dendritic cells from the skin to draining LNs.

Additionally, one-year-old mice displayed multiple signs of autoimmunity. These data suggest that lymphatic drainage plays more important roles in regulating humoral immunity and peripheral tolerance than in effector T cell immunity. Inhibition of lymphangiogenesis and lymphatic drainage via VEGFR - 3 blockade increases the severity of inflammation in chronic inflammatory arthritis. Object Investigation of the effect of lymphatic inhibition on joint and draining lymph node pathology during the course of arthritis progression in mice.

The animals were subjected to near-infrared lymphatic imaging to determine the effect of VEGFR - 3 neutralization on lymph transport from paws to draining PLNs prior to sacrifice. However, it increased the synovial volumes and inflammatory area in ankle and knee joints. VEGFR-2 neutralizing antibody, in contrast, inhibited both lymphangiogenesis and joint inflammation. Conclusion Lymphangiogenesis and lymphatic drainage are reciprocally related to the severity of joint lesions during the development of chronic arthritis.

Lymphatic drainage plays a beneficial role in controlling the progression of chronic inflammation. Mesenchymal stromal cells MSCs in bone marrow may enhance tumor metastases through the secretion of chemokines. MSCs have been reported to home toward the hypoxic tumor microenvironment in vivo.

In this study, we investigated prostate cancer PC3 cell behavior under the influence of hypoxia preconditioned MSCs and explored the related mechanism of prostate cancer lymphatic metastases in mice. Knock-in Ccr7 in PC3 cells also improved cell migration in vitro. Furthermore, when PC3 cells were labeled using the hrGfp-lentiviral vector, and were combined with hypoxia preconditioned MSCs for xenografting, it resulted in an enhancement of lymph node metastases accompanied by up-regulation of VEGFR - 3 and CCR7 in primary tumors.

Our results provide the new insights into the functional molecular events and signalings influencing prostate tumor metastases, suggesting a hopeful diagnosis and treatment in new approaches. Vitamin K2 downregulates the expression of fibroblast growth factor receptor 3 in human hepatocellular carcinoma cells. Vitamin K2 exerts an antitumor activity on human hepatocellular carcinoma HCC , however, its inhibitory mechanism has not yet been clarified.

This study was designed to identify the attractive target molecule of vitamin K2 and shed some light on its effects on fibroblast growth factor receptor FGFR 3 in HCC cells. The promoter activity of the FGFR3 gene was measured by a dual-luciferase assay. Vitamin K2 suppresses the proliferation of HuH-7 in a dose-dependent manner and its inhibitory rate reached approximately The luciferase assay demonstrated that vitamin K2 significantly suppressed the promoter activity of FGFR3.

Molecular modeling study of the induced-fit effect on kinase inhibition: the case of fibroblast growth factor receptor 3 FGFR3. Tyrosine kinases are a wide family of targets with strong pharmacological relevance. These proteins undergo large-scale conformational motions able to inactivate them. By the end of one of these structural processes, a new cavity is opened allowing the access to a specific type of inhibitors, called type II. The kinase domain of fibroblast growth factor receptor 3 FGFR3 falls into this family of kinases.

We describe here, for the first time, its inactivation process through target molecular dynamics. Molecular docking calculations of known ligands demonstrated that type II inhibitors are able to interact with this metastable transient conformation of FGFR3 kinase. Besides, supplemental computations were conducted and clearly show that type II inhibitors drive the kinase inactivation process through specific stabilization with the DFG triad. This induced-fit effect of type II ligands toward FGFR3 might be extrapolated to other kinase systems and provides meaningful structural information for future drug developments.

Neutral endopeptidase-resistant C-type natriuretic peptide variant represents a new therapeutic approach for treatment of fibroblast growth factor receptor 3 -related dwarfism. Achondroplasia ACH , the most common form of human dwarfism, is caused by an activating autosomal dominant mutation in the fibroblast growth factor receptor - 3 gene. Genetic overexpression of C-type natriuretic peptide CNP , a positive regulator of endochondral bone growth, prevents dwarfism in mouse models of ACH.

However, administration of exogenous CNP is compromised by its rapid clearance in vivo through receptor-mediated and proteolytic pathways. Using in vitro approaches, we developed modified variants of human CNP, resistant to proteolytic degradation by neutral endopeptidase, that retain the ability to stimulate signaling downstream of the CNP receptor, natriuretic peptide receptor B.

The variants tested in vivo demonstrated significantly longer serum half-lives than native CNP. Subcutaneous administration of one of these CNP variants BMN resulted in correction of the dwarfism phenotype in a mouse model of ACH and overgrowth of the axial and appendicular skeletons in wild-type mice without observable changes in trabecular and cortical bone architecture.

Moreover, significant growth plate widening that translated into accelerated bone growth, at hemodynamically tolerable doses, was observed in juvenile cynomolgus monkeys that had received daily subcutaneous administrations of BMN BMN was well tolerated and represents a promising new approach for treatment of patients with ACH. Atypical radiological findings in achondroplasia with uncommon mutation of the fibroblast growth factor receptor - 3 FGFR-3 gene Gly to Cys transition at codon The recent discovery of mutations in the FGFR-3 fibroblast growth factor receptor - 3 gene FGFR3 as the cause of achondroplasia has provided new insight into understanding genetic diseases.

It was surprising from the viewpoint of molecular genetics that most patients with achondroplasia showed the same mutation at nucleotide , leading to a single amino acid substitution from glycine to arginine at codon GlyArg. All 39 patients examined by two groups had the GlyArg; 38 patients and the other demonstrated a G to A and a G to C transition at nucleotide , respectively.

To date, a total of patients with the mutation of the GArg have been reported; a single patient with another mutation resulting in a substitution from glycine to cysteine at codon GlyCys has been described. The presence of this common mutation is consistent with the clinical fact that achondroplastic individuals show less phenotypic variability than is unusual for autosomal dominant diseases.

We encountered a Japanese boy with the GlyCys. His mother with achondroplasia has the same mutation. The molecular investigation of these patients was reported elsewhere. Here we report the clinical and radiological findings in this boy who demonstrated some atypical manifestations from those of typical achondroplasia. Serum and synovial fluid levels of tumor necrosis factor -like ligand 1A and decoy receptor 3 in rheumatoid arthritis. Tumor heterogeneity of fibroblast growth factor receptor 3 FGFR3 mutations in invasive bladder cancer: implications for perioperative anti-FGFR3 treatment.

Fibroblast growth factor receptor 3 FGFR3 is an actionable target in bladder cancer. Preclinical studies show that anti-FGFR3 treatment slows down tumor growth, suggesting that this tyrosine kinase receptor is a candidate for personalized bladder cancer treatment, particularly in patients with mutated FGFR3. We addressed tumor heterogeneity in a large multicenter, multi-laboratory study, as this may have significant impact on therapeutic response.

FGFR3 mutation was associated with pN0 P Chimeras of the native form or achondroplasia mutant GC of human fibroblast growth factor receptor 3 induce ligand-dependent differentiation of PC12 cells. Mutations in the gene for human fibroblast growth factor receptor 3 hFGFR3 cause a variety of skeletal dysplasias, including the most common genetic form of dwarfism, achondroplasia ACH. Evidence indicates that these phenotypes are not due to simple haploinsufficiency of FGFR3 but are more likely related to a role in negatively regulating skeletal growth.

Following stable transfection in PC12 cells, which lack platelet-derived growth factor PDGF receptors, all clonal cell lines, with either type of chimera, showed strong neurite outgrowth in the presence of PDGF but not in its absence.

In addition, ligand-dependent phosphorylation of phospholipase Cgamma and Shc was also observed. All of these responses were comparable to those observed from ligand activation, such as by nerve growth factor , of the native PC12 cells used to prepare the stable transfectants. The cells with the chimera bearing the ACH mutation were more rapidly responsive to ligand with less sustained MAPK activation, indicative of a preactivated or primed condition and consistent with the view that these mutations weaken ligand control of FGFR3 function.

However, the full effect of the mutation likely depends in part on structural features of the extracellular domain. Although FGFR3 has been suggested to act as a negative regulator of long-bone growth in chrondrocytes, it produces differentiative signals similar to. Atypical chemokine receptor 3 ACKR3, synonym CXCR7 is increasingly considered relevant in neuroinflammatory conditions, in which its upregulation contributes to compromised endothelial barrier function and may ultimately allow inflammatory brain injury.

While an impact of ACKR3 has been recognized in several neurological autoimmune diseases, neuroinflammation may also result from infectious agents, including Ureaplasma species spp. Although commonly regarded as commensals of the adult urogenital tract, Ureaplasma spp. Nonetheless, clinical and in vitro data on Ureaplasma-induced inflammation are scarce. We established a cell culture model of Ureaplasma meningitis, aiming to analyze ACKR3 variances as a possible pathomechanism in Ureaplasma-associated neuroinflammation.

Fibroblast growth factors receptors FGFR are transmembrane protein tyrosine kinases involved in many cellular process, including growth, differentiation and angiogenesis. Dysregulation of FGFR enzymatic activity is associated with developmental disorders and cancers; therefore FGFRs have become attractive targets for drug discovery, with a number of agents in late-stage clinical trials.

Analysis of chemical shift changes upon inhibitor binding highlights a characteristic pattern of allosteric network perturbations that is of relevance for future drug discovery activities aimed at development of conformationally-selective FGFR inhibitors. In situ imaging of quantum dot-AZD conjugates for tracking the dynamic behavior of fibroblast growth factor receptor 3. Fibroblast growth factor receptors FGFRs play an important role in determining cell proliferation, differentiation, migration, and survival.

The FGFR-inhibitor interaction can be characterized using a new imaging probe that has strong, stable signal properties for in situ cellular imaging of the interaction without quenching. We developed a kinase-inhibitor-modified quantum dot QD probe to investigate the interaction between FGFR and potential inhibitors.

Thus, this new inhibitor-modified QD probe is a promising tool for understanding the interaction between FGFR and inhibitors and for creating future high-content, cell-based drug screening strategies. We report the results of the primary efficacy analysis. After investigators' selection of the chemotherapy backbone single-agent topotecan, weekly paclitaxel, or gemcitabine , patients were randomly assigned to also receive either placebo or pertuzumab mg loading dose followed by mg every 3 weeks.

Stratification factors were selected chemotherapy, prior antiangiogenic therapy, and platinum-free interval. The primary end point was independent review committee-assessed progression-free survival PFS. Additional end points included overall survival, investigator-assessed PFS, objective response rate, safety, patient-reported outcomes, and translational research.

Overall, patients were randomly assigned. Adding pertuzumab to chemotherapy did not significantly improve independent review committee-assessed PFS for the primary analysis stratified hazard ratio, 0. Sensitivity analyses and secondary efficacy end point results were consistent with the primary analysis.

The effect on PFS favoring pertuzumab was more pronounced in the gemcitabine and paclitaxel cohorts. No new safety signals were seen. Although the primary objective was not met, subgroup analyses showed trends in PFS favoring. Fibroblast growth factor FGF -2 and FGF receptor 3 are required for the development of the substantia nigra, and FGF-2 plays a crucial role for the rescue of dopaminergic neurons after 6-hydroxydopamine lesion.

Basic fibroblast growth factor FGF-2 is involved in the development and maintenance of the nervous system. Exogenous administration of FGF-2 increased dopaminergic DA graft survival in different animal models of Parkinson's disease. Whereas absence of FGF-2 led to significantly increased numbers of DA neurons, enhanced amount of the growth factor in mice overexpressing FGF-2 resulted in less tyrosine hydroxylase expression and a reduced DA cell density.

In a second set of experiments, the putative relevance of endogenous FGF-2 after neurotoxin application was investigated regarding the number of rescued DA neurons after partial 6-OHDA lesion. The lack of FGF-2 seems to be over compensated during development, but, after lesion, compensation mechanisms fail. Aberrant expression and function of death receptor - 3 and death decoy receptor - 3 in human cancer.

Upon the binding of these receptors with their corresponding ligands, the death domain recruits various proteins that mediate both the death and proliferation of cells. VEGI has been suggested to be a potential tumour suppressor. The inhibitory effects of VEGI on cancer are manifested in three main areas: a direct effect on cancer cells, an anti-angiogenic effect on endothelial cells, and the stimulation of dendritic cell maturation.

A recent study indicated that DR3 may be a new receptor for E-selectin, which has been reported to be associated with cancer metastasis. DcR3 is a soluble receptor, highly expressed in various tumours, which lacks an apparent transmembrane segment, prevents cytokine response through ligand binding and neutralization, and is an inhibitor of apoptosis.

The cytokine LIGHT activates various anti-tumour functions and is expected to be a promising candidate for cancer therapy. Mendell, Jeanne; Freeman, Daniel J. Background During early clinical development, prospective identification of a predictive biomarker and validation of an assay method may not always be feasible. Dichotomizing a continuous biomarker measure to classify responders also leads to challenges. We present a case study of a prospective—retrospective approach for a continuous biomarker identified after patient enrollment but defined prospectively before the unblinding of data.

An analysis of the strengths and weaknesses of this approach and the challenges encountered in its practical application are also provided. While the primary objective was to assess safety and progression-free survival PFS , a secondary objective was to determine a single predictive biomarker hypothesis to identify subjects most likely to benefit from the addition of patritumab.

Although not identified as the primary biomarker in the study protocol, on the basis of preclinical results from 2 independent laboratories, expression levels of the HER3 ligand heregulin HRG were prospectively declared the predictive biomarker before data unblinding but after subject enrollment. Other biomarkers, such as epidermal growth factor receptor EGFR mutation status, were also evaluated in an exploratory fashion.

The cutoff value for high vs. A maximum likelihood analysis was performed to evaluate the provisional cutoff. Results The subgroup of patients with high. Significance of increased expression of decoy receptor 3 in chronic liver disease. Considerable evidence has indicated that apoptosis plays an important role in hepatocyte death in chronic liver disease. However, the cellular and molecular mechanisms underlying liver regeneration in these diseases are largely unknown.

Plausibly, certain molecules expressed to counteract apoptosis might provide survival advantage of certain liver cells. Therefore, we investigated a possible expression of decoy receptor 3 of the tumour necrosis factor receptor family in chronic liver diseases since decoy receptor 3 is known to inhibit apoptosis mediated by pro-apoptotic tumour necrosis factor family ligands including Fas ligand.

A series of liver biopsies from patients with different stages of fibrosis were subjected to immunohistochemistry and in situ hybridization. Both decoy receptor 3 protein and mRNA were mainly expressed in biliary epithelial cells and infiltrating lymphocytes in the diseased livers. Most noticeably, intense decoy receptor 3 expression was observed in newly developing biliary ductules in regenerative nodules as well as dysplastic nodules of cirrhotic livers.

In addition, decoy receptor 3 secretion in hepatocellular carcinoma cells in culture was via the activation of mitogen-activated protein kinases. Decoy receptor 3 was specifically expressed in chronic liver diseases and hepatocellular carcinoma cells, and decoy receptor 3 might facilitate the survival of liver cells by exerting its anti-apoptotic activity during the progression of liver cirrhosis and hepatocarcinogenesis. Yersinia pestis targets neutrophils via complement receptor 3.

Merritt, Peter M. Yersinia species display a tropism for lymphoid tissues during infection, and the bacteria select innate immune cells for delivery of cytotoxic effectors by the type III secretion system. Yet the mechanism for target cell selection remains a mystery. Here we investigate the interaction of Yersinia pestis with murine splenocytes to identify factors that participate in the targeting process.

We find that interactions with primary immune cells rely on multiple factors. First, the bacterial adhesin Ail is required for efficient targeting of neutrophils in vivo. However, Ail does not appear to directly mediate binding to a specific cell type. Instead, we find that host serum factors direct Y. Importantly, specificity towards neutrophils was increased in the absence of bacterial adhesins due to reduced targeting of other cell types, but this phenotype was only visible in the presence of mouse serum.

Addition of antibodies against complement receptor 3 and CD14 blocked target cell selection, suggesting that a combination of host factors participate in steering bacteria toward neutrophils during plague infection. Activation of interferon regulatory factor -3 via toll-like receptor 3 and immunomodulatory functions detected in A lung epithelial cells exposed to misplaced U1-snRNA. Notably, expression of these parameters was suppressed by bafilomycin A 1 , an inhibitor of endosomal acidification, implicating endosomal TLR activation.

To assess the overall regulatory potential of U1-snRNA-activated epithelial cells on cytokine production, co-cultivation with peripheral blood mononuclear cells PBMC was performed. Evaluation of epigenetic inactivation of vascular endothelial growth factor receptors in head and neck squamous cell carcinoma.

The aim of this study was to determine the methylation status of the genes encoding the vascular endothelial growth factor receptors and to evaluate the usefulness of VEGFR methylation as a prognostic indicator in head and neck squamous cell carcinoma. VEGFR messenger RNA expression and promoter methylation were examined in a panel of cell lines via quantitative reverse transcription and methylation-specific polymerase chain reaction, respectively.

Promoter methylation was compared with clinical characteristics in head and neck squamous cell carcinoma samples. Methylation of the VEGFR promoters predicts poor prognosis in head and neck squamous cell carcinoma patients. The newest member of the VEGF family.

In this issue of Blood, Singh et al establish the existence of a new soluble isoform of vascular endothelial growth factor receptor 3 s VEGFR - 3 , which is synthesized and secreted by corneal epithelial cells; they show that s VEGFR - 3 modulates lymphangiogenesis by impounding vascular endothelial growth factor VEGF C and rendering it unable to activate its cognate receptors, thereby maintaining the natural alymphatic disposition of the cornea.

Davydova, Natalia; Harris, Nicole C. This mutant may be useful for developing protein-based therapeutics to drive lymphangiogenesis in clinical settings, such as lymphedema. Decoy receptor 3 promotes cell adhesion and enhances endometriosis development. Aberrant adhesion of endometrium is the essential step in the progression of endometriosis, but the molecular mechanism of ectopic growth of endometrium is still unclear. In a multivariate regression model, DcR3 expression level was the most significant parameter associated with endometriosis severity.

In vivo investigation further showed that DcR3 promoted the growth and spread of endometrium, whereas knockdown of DcR3 by lentivirus-delivered short hairpin RNA inhibited ectopic adhesion of endometrium and abrogated endometriosis progression. These observations are in support of DcR3 playing a critical role in the pathogenesis of endometriosis, and the inhibition of DcR3 expression being a promising approach for the treatment of endometriosis.

Structural basis of ligand interaction with atypical chemokine receptor 3. Chemokines drive cell migration through their interactions with seven-transmembrane 7TM chemokine receptors on cell surfaces. This receptor is upregulated in numerous cancers making it a potential drug target. Here we collected over distinct structural probes from radiolytic footprinting, disulfide trapping, and mutagenesis to map the structures of ACKR3:CXCL12 and ACKR3:small-molecule complexes, including dynamic regions that proved unresolvable by X-ray crystallography in homologous receptors.

The data are integrated with molecular modelling to produce complete and cohesive experimentally driven models that confirm and expand on the existing knowledge of the architecture of receptor:chemokine and receptor:small-molecule complexes.

Additionally, we detected and characterized ligand-induced conformational changes in the transmembrane and intracellular regions of ACKR3 that elucidate fundamental structural elements of agonism in this atypical receptor. Serum decoy receptor 3 , a potential new biomarker for sepsis.

Sepsis, a common deadly systemic infection caused by a variety of pathogens, has some clinical symptoms similar to the systemic inflammatory response syndrome SIRS , a whole-body non-infectious inflammatory reaction to severe insults, such as burn, trauma, hypotensive shock and so on. Treatment of sepsis depends mainly on anti-microbial, while remedy for SIRS might require steroids that could possibly enhance the spread of microbes.

Unfortunately, it is very difficult to distinguish these two completely different serious conditions without blood culture, which takes days to grow and identify causative pathogens. We examined a biomarker, serum decoy receptor 3 DcR3 , was evaluated for its utility in the differential diagnosis between sepsis and SIRS.

Invasive aspergillosis IA remains a major cause of morbidity in immunocompromised hosts. This is due to the inability of the host immunity to respond appropriately to Aspergillus. An established risk factor for IA is neutropenia that is encountered by patients undergoing chemotherapy. Herein, we investigate the role of neutrophils in modulating host response to Aspergillus.

We found that neutrophils had the propensity to suppress proinflammatory cytokine production but through different mechanisms for specific cytokines. Cellular contact was requisite for the modulation of interleukin-1 beta production by Aspergillus with the involvement of complement receptor 3. Our study illustrates the extended immune modulatory role of neutrophils beyond its primary phagocytic function. The absence of neutrophils and loss of its inhibitory effect on cytokine production explains the hypercytokinemia seen in neutropenic patients when infected with Aspergillus.

Targeted resequencing identifies defective variants of decoy receptor 3 in pediatric-onset inflammatory bowel disease. Genome-wide association studies have implicated common variation at the 20q13 locus in inflammatory bowel disease, particularly for the pediatric Crohn's form. This locus harbors tumor necrosis factor receptor superfamily TNFRSF6B , encoding a secreted protein, decoy receptor 3 DcR3 , which binds to and neutralizes pro-inflammatory cytokines of the tumor necrosis factor superfamily.

We sequenced the exons of the gene in Caucasian pediatric IBD cases and Caucasian healthy controls to establish the frequency of such events in each population. Sequencing revealed that our IBD cohort harbored a greater number of missense variants, yielding an odds ratio of 3. Using functional assays, we established that the frequency of mutants defective in secretion from cultured cells was greater in the Crohn's category than in the controls, yielding an odds ratio of 7.

Unbalanced inflammatory response and lymphocyte apoptosis is associated with high mortality in septic patients. Decoy receptor 3 DcR3 , a member of the tumor necrosis factor receptor superfamily, is an anti-inflammatory and anti-apoptotic factor. Recently, DcR3 expression was found to be increased in septic patients. This study evaluated the therapeutic effect and mechanisms of DcR3 on cecal ligation and puncture CLP -induced sepsis in mice. Bacterial clearance, cytokine production, histology, lymphocyte apoptosis and survival were evaluated.

Furthermore, we investigated the systemic effects of DcR3 in in vitro lymphocyte apoptosis regulation. Our results demonstrated that DcR3 protein treatments significantly improved survival in septic mice p A decoy receptor 3 analogue reduces localised defects in phagocyte function in pneumococcal pneumonia. Therapeutic strategies to modulate the host response to bacterial pneumonia are needed to improve outcomes during community-acquired pneumonia.

This study used mice with impaired Fas signalling to examine susceptibility to pneumococcal pneumonia and decoy receptor 3 analogue DcR3-a to correct factors associated with increased susceptibility. Wild-type mice and those with varying degrees of impairment of Fas lpr or Fas ligand signalling gld were challenged with Streptococcus pneumoniae and microbiological and immunological outcomes measured in the presence or absence of DcR3-a.

During established pneumonia, neutrophils became the predominant cell in the airway and gld mice were less able to clear bacteria from the lungs, demonstrating localised impairment of pulmonary neutrophil function in comparison to lpr or wild-type mice.

T-cells from gld mice had enhanced activation and reduced apoptosis in comparison to wild-type and lpr mice during established pneumonia. Treatment with DcR3-a reduced T-cell activation and corrected the defect in pulmonary bacterial clearance in gld mice. The results suggest that imbalance in tumour necrosis factor superfamily signalling and excessive T-cell activation can impair bacterial clearance in the lung but that DcR3-a treatment can reduce T-cell activation, restore optimal pulmonary neutrophil function and enhance bacterial clearance during S pneumoniae infection.

Soluble TL1A is sufficient for activation of death receptor 3. Death receptor 3 DR3 is a typical member of the tumor necrosis factor receptor family, and was initially identified as a T-cell co-stimulatory molecule. However, further studies revealed a more complex and partly dichotomous role for DR3 and its ligand TL1A under patho physiological conditions.

TL1A and DR3 are not only a driving force in the development of autoimmune and inflammatory diseases, but also play an important role in counteracting these processes through an increase in the number of regulatory T cells.

Ligands of the tumor necrosis factor family typically occur in two forms, membrane-bound and soluble, that can differ strikingly with respect to their efficacy in activating their corresponding receptor s. To date, this has not been addressed. Here, we show that recombinant soluble trimeric TL1A is fully sufficient to strongly activate DR3-associated pro- and anti-apoptotic signaling pathways. Identification of DR3 as a tumor necrosis factor receptor that responds to soluble ligand trimers without further oligomerization provides a basis for therapeutic exploitation of the TL1A-DR3 pathway.

Fgf receptor 3 activation promotes selective growth and expansion of occipitotemporal cortex. Background Fibroblast growth factors Fgfs are important regulators of cerebral cortex development. Fgf2, Fgf8 and Fgf17 promote growth and specification of rostromedial frontoparietal cortical areas.

Recently, the function of Fgf15 in antagonizing Fgf8 in the rostral signaling center was also reported. However, regulation of caudal area formation by Fgf signaling remains unknown. Results In mutant mice with constitutive activation of Fgf receptor 3 Fgfr3 in the forebrain, surface area of the caudolateral cortex was markedly expanded at early postnatal stage, while rostromedial surface area remained normal. Cortical thickness was also increased in caudal regions.

The expression domain and levels of Fgf8, as well as overall patterning, were unchanged. In contrast, the changes in caudolateral surface area were associated with accelerated cell cycle in early stages of neurogenesis without an alteration of cell cycle exit. Moreover, a marked overproduction of intermediate neuronal progenitors was observed in later stages, indicating prolongation of neurogenesis.

Conclusion Activation of Fgfr3 selectively promotes growth of caudolateral occipitotemporal cortex. These observations support the 'radial unit' and 'radial amplification' hypotheses and may explain premature sulcation of the occipitotemporal cortex in thanatophoric dysplasia, a human FGFR3 disorder. Together with previous work, this study suggests that formation of rostral and caudal areas are differentially regulated by Fgf signaling in the cerebral cortex.

Expression of decoy receptor 3 in kidneys is associated with allograft survival after kidney transplant rejection. Decoy receptor 3 DcR3 expression in kidneys has been shown to predict progression of chronic kidney disease. We prospectively investigated a cohort comprising 96 renal transplant recipients RTRs undergoing graft kidney biopsies.

Computer-assisted quantitative immunohistochemical staining value of DcR3 in renal tubular epithelial cells RTECs was used to determine the predictive role of DcR3 in kidney disease progression. A multivariate Cox proportional hazards model was used to assess the risk of DcR3 expression in rejected kidney grafts toward the renal end point.

In total, RTRs with kidney allograft rejection were evaluated and the median follow-up was The greater expression of DcR3 immunoreactivity in RTECs was correlated with a higher rate of the histopathological concordance of acute T cell-mediated rejection.

Compared with 65 non-progressors, 31 progressors had higher DcR3 expression HDE regardless of the traditional risk factors. Cox regression analysis showed HDE was significantly associated with the risk of renal end point with a hazard ratio of 3.

In repetitive biopsies, HDE in tissue showed rapid kidney disease progression due to persistent inflammation. Decoy receptor 3 : an endogenous immunomodulator in cancer growth and inflammatory reactions. In addition to 'decoy' function, recombinant DcR3. Fc is able to modulate the activation and differentiation of dendritic cells DCs and macrophages via 'non-decoy' action.

DcR3 is upregulated in various cancer cells and several inflammatory tissues, and is regarded as a potential biomarker to predict inflammatory disease progression and cancer metastasis. However, whether DcR3 is a pathogenic factor or a suppressor to attenuate inflammatory reactions, has not been discussed comprehensively yet. Because mouse genome does not have DcR3, it is not feasible to investigate its physiological functions by gene-knockout approach. Fc fusion protein. Upregulation of DcR3 during inflammatory reactions exerts negative-feedback to suppress inflammation, while tumor cells hijack DcR3 to prevent apoptosis and promote tumor growth and invasion.

Thus, 'switch-on' of DcR3 expression may be feasible for the treatment of inflammatory diseases and enhance tissue repairing, while 'switch-off' of DcR3 expression can enhance tumor apoptosis and suppress tumor growth in vivo.

Aberrant expression of decoy receptor 3 in human breast cancer: relevance to lymphangiogenesis. Decoy receptor 3 DcR3 , a decoy receptor against Fas ligand belonging to the tumor necrosis factor receptor superfamily, is overexpressed in some forms of cancer. It was recently reported that DcR3 could protect endothelial cells from apoptosis, implying a potential role in the development of vessels, whereas its role in the lymphangiogenesis remains unclear.

In the present study, we studied the DcR3 expression and its relationship with the lymphatic microvessel density LMVD to investigate if it played a role in the lymph metastasis of human breast cancer. Real-time polymerase chain reaction and immunohistochemistry were performed to measure the messenger RNA and protein expression of DcR3 in the breast cancer tissues, noncancerous counterparts, and axillary lymph node from 63 patients.

LMVD in these specimens was assessed by counting the D labeled-microvessels. DcR3 was overexpressed in the breast cancer tissue of 58 patients LMVD in cancer tissue and lymph nodes were both positively correlated to the aberrant expression of DcR3. Based on these findings, it is important to further explore the regulation of lymphangiogenesis operated by the reverse tumor necrosis factor signaling of DcR3.

Published by Elsevier Inc. The relationship of plasma decoy receptor 3 and coronary collateral circulation in patients with coronary artery disease. Previously, decoy receptor 3 DcR3 was found to be a potential angiogenetic factor , while the relationship of DcR3 with coronary collateral circulation formation has not been investigated.

In this study, we aimed to investigate whether plasma decoy receptor 3 levels was associated with CCC formation and evaluate its predictive power for CCC status in patients with coronary artery disease. Collateral degree was graded according to Rentrope Cohen classification.

Patients with grade 2 or 3 collateral degree were enrolled in good CCC group and patients with grade 0 or 1 collateral degree were enrolled in poor CCC group. Inflammation is closely associated with cardiovascular disease, the leading cause of mortality in patients with CKD. DcR3 levels were measured in prevalent hemodialysis patients who were followed up from November 1, , to June 30, , for cardiovascular and all-cause mortality.

The baseline DcR3 concentration showed a strong positive correlation with inflammatory markers including high-sensitivity C-reactive protein, IL-6, intercellular adhesion molecule-1 ICAM-1 , and vascular cell adhesion molecule-1 VCAM During a follow-up period of 54 months, 90 patients died 34 cardiovascular deaths.

Kaplan-Meier survival analysis showed higher cardiovascular and all-cause mortality in patients with higher DcR3 levels. Based on the minimal increase in the area under the receiver operating characteristic curve from 0. Higher DcR3 levels strongly correlate with inflammation and independently predict cardiovascular and all-cause mortality in CKD patients on hemodialysis.

Interaction between geriatric nutritional risk index and decoy receptor 3 predicts mortality in chronic hemodialysis patients. Protein-energy wasting PEW is common and associated with poor outcome in hemodialysis patients. In hemodialysis patients, geriatric nutritional risk index GNRI and decoy receptor 3 DcR3 have been shown as the nutritional and inflammatory markers, respectively.

A prospective cohort of hemodialysis patients was conducted with a median follow-up of 54 months. Endpoints were cardiovascular and all-cause mortality. For patients with age factors , GNRI together with DcR3 further significantly improved the predictability for overall mortality c statistic, 0. Further studies are needed to verify whether timely recognition of hemodialysis patients with a high malnutrition-inflammation risk could reduce their mortality by appropriate interventional strategies.

Decoy receptor 3 regulates the expression of various genes in rheumatoid arthritis synovial fibroblasts. Previous studies have suggested that DcR3 acting as a ligand directly induces the differentiation of macrophages into osteoclasts. The profiles showed that among the genes most significantly regulated by DcR3, 45 were upregulated and 55 were downregulated.

The upregulated genes were associated with protein complex assembly, cell motility, regulation of transcription, cellular protein catabolic processes, cell membrane, nucleotide binding and glycosylation. The downregulated genes were associated with transcription regulator activity, RNA biosynthetic processes, cytoskeleton, zinc finger region, protein complex assembly, phosphate metabolic processes, mitochondrion, ion transport, nucleotide binding and cell fractionation.

Further study of the genes detected in the current study may provide insight into the pathogenesis and treatment of rheumatoid arthritis by DcR3-TL1A signaling. Experimental cut-offs for baseline measures determined using a graphic method were: 3. Validation of these results is warranted.

Our previous studies have shown that prior exposure of respiratory epithelial cells to an aqueous-trapped solution of DE DEas enhances the susceptibility to Influenza infections. Decoy receptor 3 : a pleiotropic immunomodulator and biomarker for inflammatory diseases, autoimmune diseases and cancer. Initial studies demonstrated that DcR3 expression is elevated in tumors cells; however, later work showed that DcR3 expression is also upregulated in inflammatory diseases, where serum DcR3 levels correlate with disease progression.

In addition to its neutralizing effect, DcR3 also acts as an effector molecule to modulate cell function via 'non-decoy' activities. This review focuses on the immunomodulatory effects of DcR3 via 'decoy' and 'non-decoy' functions, and discusses the potential of DcR3 as a biomarker to predict cancer invasion and inflammation progression. We also discuss the possible utility of recombinant DcR3 as a therapeutic agent to control autoimmune diseases, as well as the potential to attenuate tumor progression by inhibiting DcR3 expression.

Decoy receptor 3 analogous supplement protects steatotic rat liver from ischemia-reperfusion injury. For steatotic livers, pharmacological approaches to minimize the hepatic neutrophil and macrophage infiltration, and cytokine and chemokine release in ischemia-reperfusion IR injury are still limited. Conversely, anti-inflammatory M2 macrophages produce Th2 cytokine interleukin-4 , which reciprocally enhances M2 polarization.

Toll-like receptor 4-activated KCs can release proinflammatory mediators, skew M1 polarization and escalate liver IR injury. Decoy receptor 3 DcR 3 could be potential agents simultaneously blocking the IR liver injury-related pathogenic changes and extend the survival of steatotic graft. In the Zucker rat-focused experiments, various serum and hepatic substances, M1 polarization, and hepatic microcirculation were assessed.

Background: Decoy receptor 3 DcR3 is a protein with anti-apoptotic effect that belongs to the tumor necrosis factor receptor superfamily. DcR3 is highly expressed in a variety of malignant tumors including cholangiocarcinoma and its expression was found to be related to the clinical stage, the invasion, and the metastasis of the tumor. This in vitro study aimed to investigate the effect of downregulated expression of DcR3 on cell viability, cell apoptosis, and cell cycle in cholangiocarcinoma cell line TFK The cholangiocarcinoma cell line with the highest expression of DcR3 was selected for further investigation.

Various biological phenotype parameters such as cell viability, apoptosis, and cell cycle were observed. The expression of serotonin in RA or OA synovial tissue was detected using immunohistochemistry. These results suggested that synovial serotonin may be involved in the pathogenesis of RA, and that TPH1 and DcR3 may be potential therapeutic targets for the treatment of RA.

Decoy receptor 3 DcR3 is a protein with anti-apoptotic effect that belongs to the tumor necrosis factor receptor superfamily. Spinal cord injury SCI causes loss of neurons and axons and results in motor and sensory function impairments. SCI elicits an inflammatory response and induces the infiltration of immune cells, predominantly macrophages, to the injured site.

Decoy receptor 3 DcR3 , also known as tumor necrosis factor receptor superfamily member TNFRSF -6B, is a pleiotropic immunomodulator capable of inducing macrophage differentiation into the M2 phenotype and enhancing angiogenesis. Because M2 macrophages are crucial for the recovery of impaired motor functions, we ask whether DcR3 is beneficial for the functional recovery of locomotion in Sprague-Dawley SD rats after SCI.

The cavity size and myelin sparing in the rostral-to-caudal region, including the epicenter of the injury, were then examined in SCI rats by histological staining. Statistical analysis was performed using a two-tailed Student's t test. Intrathecal administration of DcR3. Fc significantly improved locomotor function and reduced secondary injury with a smaller wound cavity and increased myelin sparing at the lesion site.

Compared with the control group, DcR3. Fc-treated rats at day 7 after SCI. Moreover, higher levels of arginase I Arg I. Serum decoy receptor 3 is a biomarker for disease severity in nonatopic asthma patients. Decoy receptor 3 DcR3 , a soluble receptor of the tumor necrosis factor receptor superfamily, is a pleiotropic immunomodulator. The aim of this study was to investigate serum DcR3 levels in atopic and nonatopic asthma patients. The asthma patients were divided into atopic and nonatopic subgroups, based on the presence or absence of immunoglobulin E IgE specific to allergen.

The mean serum DcR3 level was significantly higher in asthma patients than in healthy controls High serum DcR3 levels are associated with disease severity in nonatopic asthma patients, which suggests that DcR3 is a potential biomarker that can be used to predict the severity of nonatopic asthma.

Published by Elsevier B. Sphingosine 1-phosphate receptor 3 regulates recruitment of anti-inflammatory monocytes to microvessels during implant arteriogenesis. Awojoodu, Anthony O. Endothelial cells play significant roles in conditioning tissues after injury by the production and secretion of angiocrine factors. We demonstrate here that local sphingosine 1-phosphate receptor 3 S1P3 agonism recruits anti-inflammatory monocytes to remodeling vessels.

The altered balance of cytokine secretion results in preferential recruitment of anti-inflammatory monocytes from circulation. FTY delivery enhanced arteriolar diameter expansion and increased length density of the local vasculature. This work establishes a role for S1P receptor signaling in the local conditioning of tissues by angiocrine factors that preferentially recruit regenerative monocytes that can enhance healing outcomes, tissue regeneration, and biomaterial implant functionality.

Changes in regulatory molecules for lymphangiogenesis in intestinal lymphangiectasia with enteric protein loss. We investigated the expression of regulatory molecules for lymphangiogenesis in the duodenal mucosa of idiopathic intestinal lymphangiectasia.

Biopsy samples were obtained from duodenal biopsies in patients with intestinal lymphangiectasia complicated with protein-losing from white spot lesions in which lymphangiectasia was histologically confirmed. In the control mucosa, VEGFR 3 was weakly expressed on the central lymphatic vessels in the lamina propria and LYVE-1 was expressed mainly on the lymphatic vessels in the submucosa.

In intestinal lymphangiectasia, VEGFR 3 and LYVE-1 expression levels were increased on the mucosal surface corresponding to widely dilated lymphatic vessels, while they were decreased in the deeper mucosa. There is an altered expression of regulatory molecules for lymphangiogenesis in the duodenal mucosa in these patients. Vascular lesions of the orbit, although not malignant, can cause morbidity because of their location near critical structures in the orbit. For the same reason, they can be challenging to remove surgically.

Anti-vascular endothelial growth factor VEGF drugs are increasingly being used to treat diseases with prominent angiogenesis. Our study aimed to determine to what extent VEGF receptors and their subtypes are expressed on selected vascular lesions of the orbit.

Retrospective case series of all orbital vascular lesions removed by one of the authors JAG at the Mayo Clinic. A total of 52 patients who underwent removal of vascular orbital lesions. The pathology specimens from the patients were retrieved, their pathologic diagnosis was confirmed, demographic and clinical information were gathered, and sections from vascular tumors were stained with vascular endothelial growth factor receptor VEGFR , vascular endothelial growth factor receptor type 1 VEGFR1 , vascular endothelial growth factor receptor type 2 VEGFR2 , and vascular endothelial growth factor receptor type 3 VEGFR 3.

The existence and pattern of staining with VEGF and its subtypes on these lesions. There were 28 specimens of venous malformations, 4 capillary hemangiomas, 7 lymphatic malformations, and 6 lymphaticovenous malformations. Most orbital vascular lesions express VEGF receptors, which may suggest a future target for nonsurgical treatment. Decoy receptor 3 DcR3 , a member of the tumor necrosis factor receptor TNFR superfamily, shows inhibitory effects on Fas-mediated apoptosis.

Currently, data are lacking on the correlation between DcR3 and the recurrence of breast cancer. The authors examined DcR3 mRNA expression and genomic amplification in breast cancer, and investigated the effect of DcR3 gene amplification on prognosis of patients. A total of 95 patients formed the basis of the current retrospective study.

DcR3 gene amplification was examined by quantitative polymerase chain reaction. The correlation between DcR3 gene amplification status and clinicopathological factors was examined and also the relationship between DcR3-Amp and relapse and survival. However, there was no correlation between the remaining clinicopathological factors and DcR3 gene amplification. There were no significant differences in serum IL, IL, and TL1A levels among the active-vasculitis patients, inactive-vasculitis patients, and controls.

Elevated serum levels of decoy receptor 3 are associated with disease severity in patients with hemorrhagic fever with renal syndrome. Hemorrhagic fever with renal syndrome HFRS is an acute viral infectious disease characterized by fever, hemorrhage and renal failure. HFRS has become a serious public health problem in China. Unfortunately, the pathogenesis of HFRS has not been completely clarified. The aim of this study is to investigate the changes of decoy receptor 3 DcR3 and to further explore its potential roles in HFRS.

We found serum DcR3 levels increased significantly, which reached peak value during the oliguric phase and in the critical group. This study indicates that high levels of serum DcR3 have associations with the disease stages, severity and degree of kidney damage. First, DcR3 is involved in the inflammatory cascade response resulting in capillary permeability and kidney injury in the early stage.

Secondly, HTNV infection induced DcR3 expression at the convalescent phase may act as a feed-back mechanism in anti-inflammatory response. Serum decoy receptor 3 level: a predictive marker for nodal metastasis and survival among oral cavity cancer patients. Validating markers for prediction of nodal metastasis could be beneficial in treatment of oral cavity cancer. Decoy receptor 3 DcR3 , locus on 20q13, functions as a death decoy inhibiting apoptosis mediated by the tumor necrosis factor receptor TNFR family.

This study analyzed the serum level of DcR3 in relationship to the clinical parameters of oral cavity cancer patients together with detection of DcR3 genomic copy number in primary and recurrent tumors. Elevated serum DcR3 was associated with nodal metastasis and worse prognosis.

Serum DcR3 level is a predictor for the nodal metastasis and survival among oral cavity cancer patients and the DcR3 copy number alteration could underlie oral carcinogenesis progression. Decoy receptor 3 polymorphisms are not associated with the risk of esophageal cancer in a Chinese population.

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