Vascular endothelial growth factor (VEGF) and its receptors

  title={Vascular endothelial growth factor (VEGF) and its receptors},
  author={Gera Neufeld and Tzafra Cohen and Stela Gengrinovitch and Zoya Poltorak},
  journal={The FASEB Journal},
  pages={22 - 9}
Vascular endothelial growth factor (VEGF) is a highly specific mitogen for vascular endothelial cells. Five VEGF isoforms are generated as a result of alternative splicing from a single VEGF gene. These isoforms differ in their molecular mass and in biological properties such as their ability to bind to cell‐surface heparan‐sulfate proteoglycans. The expression of VEGF is potentiated in response to hypoxia, by activated oncogenes, and by a variety of cytokines. VEGF induces endothelial cell… 

Vascular endothelial growth factor: basic science and clinical progress.

Vascular endothelial growth factor (VEGF) is an endothelial cell-specific mitogen in vitro and an angiogenic inducer in a variety of in vivo models and is implicated in intraocular neovascularization associated with diabetic retinopathy and age-related macular degeneration.

Vascular Endothelial Growth Factor Family and Its Receptors

A large body of experimental evidence has established VEGF as an essential molecule in promoting angiogenesis during tumor growth and the development of therapeutic agents that selectively target various VEGf ligands and their receptors are emphasized.

Expression of Vascular Endothelial Growth Factor (VEGF) and VEGF Receptors in Tumor Angiogenesis and Malignancies

Therapeutic inhibition of vessel formation could be best suited to preventive strategies aimed at the suppression of angiogenesis in primary tumors in subjects at risk or of micrometastases after surgical removal of primary tumor.

Vascular endothelial growth factor (VEGF) - key factor in normal and pathological angiogenesis.

This article aims to highlight the most recent data referring to the VEGF family and its receptors, as well as its implications in the angiogenesis process.

Functional Significance of Vascular Endothelial Growth Factor Receptor Expression on Human Glioma Cells

VEGF or the VEGFR agonists VEGF-D or placenta growth factor (PlGF) did not produce significant effects on glioma cell proliferation or V EGF production and functional effects are low and autocrine growth stimulatory effects within a gliomas are minor.

Connective tissue growth factor binds vascular endothelial growth factor (VEGF) and inhibits VEGF‐induced angiogenesis

  • I. InokiT. Shiomi Y. Okada
  • Biology, Chemistry
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • 2002
It is demonstrated for the first time that VEGF165 binds to CTGF through a protein‐to‐protein interaction and suggest that the angiogenic activity of V EGF165 is regulated negatively by CTGF in the extracellular environment.

Role of the vascular endothelial growth factor pathway in tumor growth and angiogenesis.

  • D. HicklinL. Ellis
  • Biology
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • 2005
Recently, an anti-VEGF antibody (bevacizumab), when used in combination with chemotherapy, was shown to significantly improve survival and response rates in patients with metastatic colorectal cancer and thus, validate VEGF pathway inhibitors as an important new treatment modality in cancer therapy.

Synergism between vascular endothelial growth factor and placental growth factor contributes to angiogenesis and plasma extravasation in pathological conditions

It is reported that embryonic angiogenesis in mice was not affected by deficiency of PlGF, andTransplantation of wild-type bone marrow rescued the impairedAngiogenesis and collateral growth in Pgf−/− mice, indicating that PlGF might have contributed to vessel growth in the adult by mobilizing bone-marrow–derived cells.

VEGF165b, an Inhibitory Vascular Endothelial Growth Factor Splice Variant

It is shown that an endogenous splice variant, VEGF165b, is expressed as protein in normal cells and tissues and is circulating in human plasma, and that it inhibits VEGf165-mediated angiogenesis in rabbit cornea and rat mesentery, suggesting that regulation of V EGF splicing may be a critical switch from an antiangiogenic to a proangiogenesis phenotype.

VEGF-VEGF receptor complexes as markers of tumor vascular endothelium.

  • R. BrekkenP. Thorpe
  • Biology, Chemistry
    Journal of controlled release : official journal of the Controlled Release Society
  • 2001



VEGF145, a Secreted Vascular Endothelial Growth Factor Isoform That Binds to Extracellular Matrix*

Recombinant VEGF145 induced the proliferation of vascular endothelial cells and promoted angiogenesis in vivo and seems to possess a unique combination of biological properties distinct from those of previously characterized V EGF species.

Inhibition of tumor growth by targeting tumor endothelium using a soluble vascular endothelial growth factor receptor.

  • P. LinS. Sankar K. Peters
  • Biology, Medicine
    Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research
  • 1998
The potential of ExFlk.6His to inhibit VEGF action by a potent "dominant-negative" mechanism is demonstrated and targeting V EGF action using a soluble receptor may be an effective antiangiogenic therapy for cancer and other "angiogenesis" diseases.

Selective Binding of VEGF to One of the Three Vascular Endothelial Growth Factor Receptors of Vascular Endothelial Cells (*)

Experiments suggest that alternative splicing can generate a diversity in growth factor signaling by determining receptor recognition patterns and indicate that the heparin binding ability of VEGF may enable the restoration of damaged V EGF function in processes such as inflammation or wound healing.

Patterns of expression of vascular endothelial growth factor (VEGF) and VEGF receptors in mice suggest a role in hormonally regulated angiogenesis.

It is proposed that excessive expression of VEGF during gonadotropin-induced ovulation may contribute to the development of ovarian hyperstimulation syndromes by virtue of the vascular permeabilization activity of this factor.

Dual regulation of vascular endothelial growth factor bioavailability by genetic and proteolytic mechanisms.

Vascular endothelial growth factor up-regulates its receptor fms-like tyrosine kinase 1 (FLT-1) and a soluble variant of FLT-1 in human vascular endothelial cells.

It is shown that media conditioned by various cancer cell lines grown under hypoxic conditions were able to up-regulate expression of FLT-1 mRNA and protein but not of KDR mRNA, which suggests that VEGF itself is the main factor secreted by tumor cells that is able to enhance the expression of its receptor FLt-1 and of a soluble variant of FLS-1 in endothelial cells.

Vascular endothelial growth factors VEGF‐B and VEGF‐C

The role of VEGF in embryogenesis is emphasized by the unprecedented result that the inactivation of even a generated by alternative splicing of mRNA from the V EGF-B gene, spanning about 4 kb of DNA, is emphasized.

Inhibition of Vascular Endothelial Growth Factor (VEGF)-induced Endothelial Cell Proliferation by a Peptide Corresponding to the Exon 7-Encoded Domain of VEGF165 *

It was concluded that the exon 7-encoded domain of V EGF165 enhances its mitogenic activity for HUVEC by interacting with VEGF165R and modulating KDR/Flk-1-mediated mitogenicity indirectly and that exon 6-derived peptides may be useful VEGf antagonists in angiogenesis-associated diseases.

Vascular permeability factor/vascular endothelial growth factor: a multifunctional angiogenic cytokine.

VPF/VEGF has taught us something new about angiogenesis; namely, that vascular hyperpermeability and consequent plasma protein extravasation are important--perhaps essential--elements in its generation, however, this finding raises a paradox.