Activation initiates intracellular signal pathways within endothelial cells that promote proliferation, migration and survival of endothelium.
A critical rate limiting molecule in angiogenesis.
Regulates vascular development, blood vessel function and lymph vessel function.
Soluble growth factors that can be secreted by tumors cells.
Requires during embryological growth and development and without which death would ensue.
A heparin binding glycoprotein family includes 6 members VEG A-E and PDGF.
Also ref2242ed to as VEGF-A
VEGF-A is a key regulator of both physiologic and pathologic angiogenesis.
VEGF-A most prominent mediator of tumor angiogenesis.
Splicing of the 8 exons of the VEGF-A gene results in the synthesis of six different human isoforms, with VEGF165 the most common isoform and most important for angiogenesis.
A polypeptide found on chromosome 6p12.
The VEGF gene encodes for four major isoforms 121, 165, 189, and 206 and a few less common forms 145 and 183
VEGF-C and VEFF-D. are involved in the regulation of lymphangiogenesis.
Neovascularization of tumors associated with VEGF stimulation of angiogenesis.
Cells produce this protein to stimulate the growth of new blood vessels, which promotes healing when blood vessels were injured or occluded.
Cell receptors and oncogenes contribute to increased VEGF expression.
Increases microvascular permeability, induces endothelial cell migration and division, promotes endothelial cell survival, prevents endothelial cell senescence, reprograms gene expression, and induces angiogenesis and lymph vessel angiogenesis.
Promotes the generation of extracellular matrix by endothelial cells and regulates vascular permeability to induce vascular leakage.
Upregulated in many solid tumors and is greatest in hypoxic tumor cells near necrotic areas, suggesting that hypoxia induces VEGF and is vital for the development of tumor vasculature
VEGF is controlled by hypoxia inducible factor (HIF) binds to to endothelial receptors, resulting in mitogenic, angiogenic, and pro permeability signaling.
Induces bone marrow derived endothelial progenitor cells to new vasculature.
A multifunctional cytokine that increases microvasculature permeability.
Overexpression of VEGF can lead to vascular disease or the unchecked growth of malignant tumors.
Overexpressed in most solid tumors and can be upregulated by external stimuli.
Signals angiogenesis and promotes the survival of a tumor’s existing vasculature.
Signaling of VEGF allows tumors to establish their own supporting vascular network and secures nutrients and oxygen for the tumor.
Facilitates growth in infiltration of tumors into surrounding tissues.
High levels of VEGF in a tumor’s vasculature is associated with leaky pericytes, increased permeability and tortuousness.
Formation of intratumoral microvasculature caused by VEGF may result in improved chemotherapy delivery.
High expression of VEGF predicts chemosensitivity of gastric cancer patients treated with 5 FU.
Fifty thousand times more potent than histamine in causing vascular leak and is in high concentration in the ascitic fluid of patients with malignant ascites.
Overexpression predicts a poor prognosis for ovarian cancer.
Overexpressed in lung, breast, kidney, bladder, ovary cervix, and gastrointestinal tumors.
Overexpression in lymphoma is associated with poor prognosis.
Overexpression in non-small cell lung cancer is associated with a poor prognosis.
High serum levels of VEGF correlate with chemotherapy resistnce and poor survival in small cell lung cancer (SCLC).
High levels in ovarian cancer complicated by ascites.
Levels are elevated in patients with leukemia and multiple myeloma and sometimes associated with lower rates of response to treatment, shorter duration of response and lower survival.
Elevated pretreatment levels in non-Hodgkin’s lymphoma associated with poorer survival.
Elevated levels associated with Hodgkin’s lymphoma and the elevation persists after treatment and long into sustained remission.
Pathologic neovascularization and hyper permeability in the eye can cause blindness from retinal detachment, uncontrolled glaucoma and untreatable retinal edema.
It is the principal cause of blinding chorioretinal vascular diseases
Exerts effects on vascular endothelial cell via 2 receptor tyrosine kinases VEGFR1 And VEGFR2.
VEGF binds to and activates 3 VEGFR (vascular endothelial growth factor receptors) on endothelial cells of blood vessels and lymphatics.
Increased prosuction of VEGF causes endothelial damage and can lead to endothelial changes, multiplication and spread, leading to tumor angiogenesis and tumor growth.
Infusion stimulates microvascular perfusion in patients with severe coronary artery disease and ischemic extremities.