Abstract
Angiogenesis is the development of new and small blood vessels by budding and sprouting from larger, extant vessels (Beck Jr, and D’Amore, 1997; Bussolino, Montavani, and Persico, 1997). In adult tissues endothelial cells are quiescent but rapid proliferation occurs for a limited period of time during menstruation, ovulation, reproduction, implantation, mammary gland changes during lactation, and wound healing (Cockerill, Gamble, and Vadas, 1995; Folkman, and Shing, 1992). Abnormal or uncontrolled angiogenesis has been seen in diabetic retinopathy, arthritis, hemangiomas, psoriasis as well as for growth and maintenance of many types of benign and malignant tumors (Cockerill et al, 1995; Folkman, Watson, Ingber, and Hanahan, 1989; Liotta, Stug, and Stetlen-Stevenson, 1992; Saclarides, Speziale, Drab, Szeluga, and Rubin, 1994; Folkman, 1992). Inducers of angiogenesis can act directly on endothelial cells, or indirectly, via accessory cells (monocytes, mastocytes, T cells). Vascular growth factor A (VEGF-A), VEGF-B, VEGF-C and placental growth factor (PIGF) are angiogenic glycoproteins and display high amino acid similarity in the platelet-derived growth factor (PDGF) and tumor necrosis factor α (TNF α) and requires interaction with integrins αvβ3; the other is via VEGF-A and is integrins αvβ5 — dependent (Friedlander, Brook, Shaffer, Kincaid, Verner, and Cheresh, 1995). It is also becoming evident that there are different classes of endogenous inhibitors of endothelial cell growth and motility that work in concert with inducer molecules to control angiogenesis.
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Banerjee, D.K., Martínez, J.A. (1998). Microvascular Endothelial Cells from Adrenal Medulla — A Model for in Vitro Angiogenesis. In: Maragoudakis, M.E. (eds) Angiogenesis. NATO ASI Series, vol 298. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9185-3_2
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