In vitro, VEGF-A has been shown to stimulate endothelial cell mitogenesis and cell migration.
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In vitro, VEGF-A has been shown to stimulate endothelial cell mitogenesis and cell migration.
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VEGF-A is a vasodilator and increases microvascular permeability and was originally referred to as vascular permeability factor.
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Recently, VEGF-C has been shown to be an important inducer of neurogenesis in the murine subventricular zone, without exerting angiogenic effects.
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The VEGF receptors have an extracellular portion consisting of 7 immunoglobulin-like domains, a single transmembrane spanning region, and an intracellular portion containing a split tyrosine-kinase domain.
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The expression of angiopoietin-2 in the absence of VEGF leads to endothelial cell death and vascular regression.
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VEGF-A is highly expressed in the acute and sub-acute stages of CNS injury, but the protein expression declines over time.
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VEGF-A has been implicated with poor prognosis in breast cancer.
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VEGF-A is released in rheumatoid arthritis in response to TNF-a, increasing endothelial permeability and swelling and stimulating angiogenesis.
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VEGF-A plays a role in the disease pathology of the wet form age-related macular degeneration, which is the leading cause of blindness for the elderly of the industrialized world.
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Hence, VEGF is a potential target for the treatment of cancer.
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VEGF-D has been shown to be over expressed in lymphangioleiomyomatosis and is currently used as a diagnostic biomarker in the treatment of this rare disease.
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