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Vascular endothelial growth factor A
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Vascular endothelial growth factor A
Vascular endothelial growth factor A (VEGF-A) is a protein that in humans is encoded by the VEGFA gene.
This gene is a member of the platelet-derived growth factor (PDGF)/vascular endothelial growth factor (VEGF) family and encodes a protein that is often found as a disulfide linked homodimer. This protein is a glycosylated mitogen that specifically acts on endothelial cells and has various effects, including mediating increased vascular permeability, inducing angiogenesis, vasculogenesis, and endothelial cell growth, promoting cell migration, and inhibiting apoptosis. Alternatively spliced transcript variants, encoding either freely secreted or cell-associated isoforms, have been characterized.
VEGF-A shows prominent activity with vascular endothelial cells, primarily through its interactions with the VEGFR1 and -R2 receptors found prominently on the endothelial cell membrane. However, it does have effects on a number of other cell types (e.g., stimulation monocyte/macrophage migration, neurons, cancer cells, kidney and epithelial cells ). In vitro, VEGF-A has been shown to stimulate endothelial cell mitogenesis and cell migration. VEGF-A is also a vasodilator and increases microvascular permeability and was originally referred to as vascular permeability factor.
During embryonic development angiogenesis is initiated as mesoderm mesenchyme cells are specified to differentiate into angioblasts, expressing the Vascular Endothelial Growth Factor Receptor (VEGFR-2). As embryonic tissue utilizes more oxygen than it receives from diffusion, it becomes hypoxic. These cells will secrete the signaling molecule vascular endothelial factor A (VEGFA) which will recruit the angioblasts expressing its partnering receptor to the site of future angiogenesis. The angioblasts will create scaffolding structures that form the primary capillary plexus from where the local vasculature system will develop. Disruption of this gene in mice resulted in abnormal embryonic blood vessel formation, resulting in underdeveloped vascular structures. This gene is also upregulated in many tumors and its expression is correlated with tumor development and is a target in many developing cancer therapeutics. Elevated levels of this protein are found in patients with POEMS syndrome, also known as Crow-Fukase syndrome which is a hemangioblastic proliferative disorder. Allelic variants of this gene have been associated with microvascular complications of diabetes 1 and atherosclerosis.
Vascular endothelial growth factor A (VEGF-A) is a dimeric glycoprotein that plays a significant role in neurons and is considered to be the main, dominant inducer of the growth of blood vessels. VEGFA is essential for adults during organ remodeling and diseases that involve blood vessels, for example, in wound healing, tumor angiogenesis, diabetic retinopathy, and age-related macular degeneration. During early vertebrate development, vasculogenesis occurs which means that the endothelial condense into the blood vessels. The differentiation of endothelial cells is dependent upon the expression of VEGFA and if the expression is abolished then it can result in the death of the embryo. VEGFA is produced by a group of three major isoforms as a result of alternative splicing and if any three isoforms are produced (VEGFA120, VEGFA164, and VEGFA188) then this will not result in vessel defects and death of the full VEGFA knockout in mice. VEGFA is essential in the role of neurons because they too need vascular supply and abolishing the expression of VEGFA from neural progenitors will result in defects of the brain vascularization and neuronal apoptosis. Anti-VEGFA therapy can be used to treat patients with undesirable angiogenesis and vascular leakage in cancer and eye diseases but also could result in the inhibition of neurogenesis and neuroprotection. VEGFA could be used to treat patients with neurodegenerative and neuropathic conditions and also increase vascular permeability which will stop the blood-brain barrier and increase inflammatory cell infiltration.
Also tumour suppression.
Elevated levels of this protein is linked to POEMS syndrome, also known as Crow-Fukase syndrome. Mutations in this gene have been associated with proliferative and nonproliferative diabetic retinopathy.
In ischemic cardiomyopathy, blood flow to the muscle cells of the heart is either partially or completely reduced, leading to cell death and scar tissue formation. Because the muscle cells are replaced with fibrous tissue, the heart loses its ability to contract, compromising heart function. Normally, if blood flow to the heart is compromised, over time, new blood vessels will develop, providing alternative circulation to the affected cells. The viability of the heart following severely restricted blood flow is dependent on the ability of the heart to provide this collateral circulation. Expression of VEGF-A has been found to be induced by myocardial ischemia and a higher level of expression of VEGF-A has been associated with better collateral circulation development during ischemia.
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Vascular endothelial growth factor A
Vascular endothelial growth factor A (VEGF-A) is a protein that in humans is encoded by the VEGFA gene.
This gene is a member of the platelet-derived growth factor (PDGF)/vascular endothelial growth factor (VEGF) family and encodes a protein that is often found as a disulfide linked homodimer. This protein is a glycosylated mitogen that specifically acts on endothelial cells and has various effects, including mediating increased vascular permeability, inducing angiogenesis, vasculogenesis, and endothelial cell growth, promoting cell migration, and inhibiting apoptosis. Alternatively spliced transcript variants, encoding either freely secreted or cell-associated isoforms, have been characterized.
VEGF-A shows prominent activity with vascular endothelial cells, primarily through its interactions with the VEGFR1 and -R2 receptors found prominently on the endothelial cell membrane. However, it does have effects on a number of other cell types (e.g., stimulation monocyte/macrophage migration, neurons, cancer cells, kidney and epithelial cells ). In vitro, VEGF-A has been shown to stimulate endothelial cell mitogenesis and cell migration. VEGF-A is also a vasodilator and increases microvascular permeability and was originally referred to as vascular permeability factor.
During embryonic development angiogenesis is initiated as mesoderm mesenchyme cells are specified to differentiate into angioblasts, expressing the Vascular Endothelial Growth Factor Receptor (VEGFR-2). As embryonic tissue utilizes more oxygen than it receives from diffusion, it becomes hypoxic. These cells will secrete the signaling molecule vascular endothelial factor A (VEGFA) which will recruit the angioblasts expressing its partnering receptor to the site of future angiogenesis. The angioblasts will create scaffolding structures that form the primary capillary plexus from where the local vasculature system will develop. Disruption of this gene in mice resulted in abnormal embryonic blood vessel formation, resulting in underdeveloped vascular structures. This gene is also upregulated in many tumors and its expression is correlated with tumor development and is a target in many developing cancer therapeutics. Elevated levels of this protein are found in patients with POEMS syndrome, also known as Crow-Fukase syndrome which is a hemangioblastic proliferative disorder. Allelic variants of this gene have been associated with microvascular complications of diabetes 1 and atherosclerosis.
Vascular endothelial growth factor A (VEGF-A) is a dimeric glycoprotein that plays a significant role in neurons and is considered to be the main, dominant inducer of the growth of blood vessels. VEGFA is essential for adults during organ remodeling and diseases that involve blood vessels, for example, in wound healing, tumor angiogenesis, diabetic retinopathy, and age-related macular degeneration. During early vertebrate development, vasculogenesis occurs which means that the endothelial condense into the blood vessels. The differentiation of endothelial cells is dependent upon the expression of VEGFA and if the expression is abolished then it can result in the death of the embryo. VEGFA is produced by a group of three major isoforms as a result of alternative splicing and if any three isoforms are produced (VEGFA120, VEGFA164, and VEGFA188) then this will not result in vessel defects and death of the full VEGFA knockout in mice. VEGFA is essential in the role of neurons because they too need vascular supply and abolishing the expression of VEGFA from neural progenitors will result in defects of the brain vascularization and neuronal apoptosis. Anti-VEGFA therapy can be used to treat patients with undesirable angiogenesis and vascular leakage in cancer and eye diseases but also could result in the inhibition of neurogenesis and neuroprotection. VEGFA could be used to treat patients with neurodegenerative and neuropathic conditions and also increase vascular permeability which will stop the blood-brain barrier and increase inflammatory cell infiltration.
Also tumour suppression.
Elevated levels of this protein is linked to POEMS syndrome, also known as Crow-Fukase syndrome. Mutations in this gene have been associated with proliferative and nonproliferative diabetic retinopathy.
In ischemic cardiomyopathy, blood flow to the muscle cells of the heart is either partially or completely reduced, leading to cell death and scar tissue formation. Because the muscle cells are replaced with fibrous tissue, the heart loses its ability to contract, compromising heart function. Normally, if blood flow to the heart is compromised, over time, new blood vessels will develop, providing alternative circulation to the affected cells. The viability of the heart following severely restricted blood flow is dependent on the ability of the heart to provide this collateral circulation. Expression of VEGF-A has been found to be induced by myocardial ischemia and a higher level of expression of VEGF-A has been associated with better collateral circulation development during ischemia.
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