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Efficient activation of the lymphangiogenic growth factor VEGF-C requires the C-terminal domain of VEGF-C and the N-terminal domain of CCBE1.
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As shown in mouse model of kidney fibrosis CTGF is significantly involved in fibrosis-associated renal lymphangiogenesis through regulation of, and direct interaction with, VEGF-C.
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Fluid shear stress regulates vascular remodeling via VEGFR-3 activation, independently of its ligand, VEGF-C, in the uterus during pregnancy.
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A novel heparin conjugate (LHbisD4) is shown to prevent lymphangiogenesis by blocking the vascular endothelial growth factor C (VEGF-C) induced signaling pathway.
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lymphangiogenesis is regulated by two distinct proteolytic mechanisms of ligand activation: one in which VEGFC activation by ADAMTS3 and CCBE1 spatially and temporally patterns developing lymphatics, and one in which VEGFD activation by a distinct proteolytic mechanism may be stimulated during inflammatory lymphatic growth
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These results reveal an unexpected role for VEGF-C, a major lymphangiogenic growth factor, in the transition to fetal liver erythropoiesis.
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Results suggest that interleukin-6 (IL-6) increases VEGF-C induction and lymphangiogenesis may involve, at least in part, Src-FAK-STAT3 cascade in lymphatic endothelial cells (LECs).
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Data show that heparanase-1 (HPA-1) induced shedding of heparan sulfate chain from syndecan-1 (SDC-1) facilitated the release of vascular endothelial growth factor C (VEGF-C) from SDC-1/VEGF-C complex into the medium of hepatocarcinoma cell.
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Data show that in the MCF-7 breast cancer cell line, only MT1X metallothioneins (MTs) positively correlated with vascular endothelial growth factor C (VEGFC).
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The findings in this study strongly suggest the following: i) that VEGF-C promotes the proliferative activity and migratory ability of mesenchymal stem cell ; and ii) VEGF-C and Tgfb reciprocally regulate mesenchymal stem cell commitment to differentiation into lymphatic endothelial or osteoblastic phenotypes, respectively.
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The authors show that VEGF-C is necessary for perinatal lymphangiogenesis, but required for adult lymphatic vessel maintenance only in the intestine.
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MT1-MMP directly cleaves LYVE-1 on lymphatic endothelial cells to inhibit LYVE-1-mediated lymphangiogenic responses and restrains the production of VEGF-C.
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HA increases lymphangiogenesis in renal fibrosis model and also stimulates vascular endothelial cell growth factor-C production from macrophages through Toll-like receptor 4-dependent signal pathway
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Results showed that the VEGF-C/VEGFR-3 system underlies the protective effect of ischemic preconditioning against forebrain ischemia in the mouse hippocampus
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Vascular endothelial growth factor C/VEGFR-3 signaling modifies HS and CCL21 gradients around lymphatics, regulating lymphocyte migration.
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Coronary artery stem development first requires VEGF-C to stimulate vessel growth around the outflow tract.
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Data show that the expression of lymphatic vessel endothelial hyaluronan receptor 1 (LYVE 1) was similar with vascular endothelial growth factor C (VEGF-C), but its peak appeared 1-2 d later than that of VEGF-C.
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reveal the evolutionary conservation of the lymphatic-like phenotype of the Schlemm's canal (SC), implicate VEGF-C and VEGFR-3 as critical regulators of SC lymphangiogenesis
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Sinus venosus-derived and endocardial-derived migratory routes unite to form the coronary vasculature, with the former requiring VEGFC - a tissue-specific mediator of blood endothelial development.
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suggest that correction of defective lymphatic function with VEGF-C has potential as a therapeutic strategy for inflammatory bowel disease.
