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MeSH Review:

Neovascularization, Physiologic

Hiratsuka, S. et al., Ishida, S. et al., Goede, V. et al., Pepper, M.S. et al., Amano, H. et al., et al.

Järvelä, Sladkevicius, Kelly, Ojha, Campbell, Nargund, Breier,

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High impact information on Neovascularization, Physiologic

Vascular endothelial growth factor (VEGF) is a key regulator of physiological angiogenesis during embryogenesis, skeletal growth and reproductive functions [1].
In contrast, administration of a VEGFR-1/Fc fusion protein, which blocks all VEGF isoforms, led to significant suppression of both pathological and physiological neovascularization [2].
In parallel experiments, genetically altered VEGF164-deficient (VEGF120/188) mice exhibited no difference in physiological neovascularization when compared with wild-type (VEGF+/+) controls [2].
Thus, VEGF-C may regulate physiological angiogenesis and participate in the development and progression of angiogenic diseases in addition to lymphangiogenesis [3].
In vivo patterns of expression of urokinase and its inhibitor PAI-1 suggest a concerted role in regulating physiological angiogenesis [4].

Biological context of Neovascularization, Physiologic

Vascular endothelial growth factor (VEGF)-mediated physiological angiogenesis results from the concerted action of three major VEGF isoforms (VEGF121, 165, 189), which arise from alternate splicing [5].

Anatomical context of Neovascularization, Physiologic

OBJECTIVE: The growth of the follicles induced by gonadotropins during IVF treatment is accompanied by physiologic angiogenesis, which is essential for the maturation of the oocytes [6].
Modulation of physiological angiogenesis in skeletal muscle by mechanical forces: involvement of VEGF and metalloproteinases [7].

Associations of Neovascularization, Physiologic with chemical compounds

Of all the different organs, the cyclic corpus luteum of the ovary is the organ site with the strongest physiological angiogenesis [8].

Gene context of Neovascularization, Physiologic

Recently, we and others have shown that Flt-1 has a negative regulatory function for physiological angiogenesis in the embryo, possibly with its strong VEGF-trapping activity [9].
Role of vascular endothelial growth factor in regulation of physiological angiogenesis [10].
In the vasculature of the adult organism, the high-affinity signaling VEGF receptor-2 (VEGFR-2) is downregulated but is reinduced during transient phases of physiological angiogenesis [11].
These findings are discussed in the context of recent observations on uPA-, uPAR-, PAI-1 and plaminogen-deficient mice, in which developmental and physiological angiogenesis appear to occur normally [12].
Our data show that MCP-1 is an indirect inflammation-associated inducer of angiogenesis and demonstrate distinct qualitative differences between tumor angiogenesis in human mammary tumors and physiological angiogenesis in the ovary [13].

References

The biology of VEGF and its receptors. Ferrara, N., Gerber, H.P., LeCouter, J. Nat. Med. (2003) [Pubmed]
VEGF164-mediated inflammation is required for pathological, but not physiological, ischemia-induced retinal neovascularization. Ishida, S., Usui, T., Yamashiro, K., Kaji, Y., Amano, S., Ogura, Y., Hida, T., Oguchi, Y., Ambati, J., Miller, J.W., Gragoudas, E.S., Ng, Y.S., D'Amore, P.A., Shima, D.T., Adamis, A.P. J. Exp. Med. (2003) [Pubmed]
Vascular endothelial growth factor C induces angiogenesis in vivo. Cao, Y., Linden, P., Farnebo, J., Cao, R., Eriksson, A., Kumar, V., Qi, J.H., Claesson-Welsh, L., Alitalo, K. Proc. Natl. Acad. Sci. U.S.A. (1998) [Pubmed]
In vivo patterns of expression of urokinase and its inhibitor PAI-1 suggest a concerted role in regulating physiological angiogenesis. Bacharach, E., Itin, A., Keshet, E. Proc. Natl. Acad. Sci. U.S.A. (1992) [Pubmed]
Alteration of splicing signals in a genomic/cDNA hybrid VEGF gene to modify the ratio of expressed VEGF isoforms enhances safety of angiogenic gene therapy. Amano, H., Hackett, N.R., Kaner, R.J., Whitlock, P., Rosengart, T.K., Crystal, R.G. Mol. Ther. (2005) [Pubmed]
Comparison of follicular vascularization in normal versus polycystic ovaries during in vitro fertilization as measured using 3-dimensional power Doppler ultrasonography. Järvelä, I.Y., Sladkevicius, P., Kelly, S., Ojha, K., Campbell, S., Nargund, G. Fertil. Steril. (2004) [Pubmed]
Modulation of physiological angiogenesis in skeletal muscle by mechanical forces: involvement of VEGF and metalloproteinases. Brown, M.D., Hudlicka, O. Angiogenesis (2003) [Pubmed]
Vascular morphogenesis in the ovary. Augustin, H.G. Baillière's best practice & research. Clinical obstetrics & gynaecology. (2000) [Pubmed]
Involvement of Flt-1 tyrosine kinase (vascular endothelial growth factor receptor-1) in pathological angiogenesis. Hiratsuka, S., Maru, Y., Okada, A., Seiki, M., Noda, T., Shibuya, M. Cancer Res. (2001) [Pubmed]
Role of vascular endothelial growth factor in regulation of physiological angiogenesis. Ferrara, N. Am. J. Physiol., Cell Physiol. (2001) [Pubmed]
Functions of the VEGF/VEGF receptor system in the vascular system. Breier, G. Semin. Thromb. Hemost. (2000) [Pubmed]
Angiogenesis: a paradigm for balanced extracellular proteolysis during cell migration and morphogenesis. Pepper, M.S., Montesano, R., Mandriota, S.J., Orci, L., Vassalli, J.D. Enzyme Protein (1996) [Pubmed]
Induction of inflammatory angiogenesis by monocyte chemoattractant protein-1. Goede, V., Brogelli, L., Ziche, M., Augustin, H.G. Int. J. Cancer (1999) [Pubmed]

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