Enenstein J, Waleh N S, Kramer R H
Department of Anatomy, University of California, San Francisco 94143.
Exp Cell Res. 1992 Dec;203(2):499-503. doi: 10.1016/0014-4827(92)90028-7.
Basic fibroblast growth factor (bFGF) and transforming growth factor-beta (TGF-beta) are known to alter the migratory and proliferative capacity of endothelial cells in vitro and to stimulate angiogenesis in vivo. One mechanism by which these cytokines induce their effects may be through the regulation of integrin adhesion receptor expression and activity. We examined the ability of these growth factors to modulate the expression of specific integrins in human microvascular endothelial cells (MEC). Immunoprecipitation of metabolically labeled MEC showed that bFGF upregulated the biosynthesis of alpha 2, alpha 5, beta 1, and beta 3. bFGF induced an increase in the levels of mRNA for alpha 2 and beta 1. TGF-beta increased synthesis of alpha 2, alpha 5, and beta 1. These results suggest that bFGF and TGF-beta selectively alter integrin profiles and influence interactions of MEC with the extracellular matrix during neovascularization. In particular, the upregulation of the collagen/laminin receptor, alpha 2 beta 1, by bFGF may provide activated endothelial cells with an enhanced capacity to migrate through both their underlying basement membrane and the interstitial matrix.
已知碱性成纤维细胞生长因子(bFGF)和转化生长因子-β(TGF-β)可在体外改变内皮细胞的迁移和增殖能力,并在体内刺激血管生成。这些细胞因子发挥作用的一种机制可能是通过调节整合素黏附受体的表达和活性。我们研究了这些生长因子调节人微血管内皮细胞(MEC)中特定整合素表达的能力。对经代谢标记的MEC进行免疫沉淀显示,bFGF上调了α2、α5、β1和β3的生物合成。bFGF诱导α2和β1的mRNA水平升高。TGF-β增加了α2、α5和β1的合成。这些结果表明,bFGF和TGF-β在新生血管形成过程中选择性地改变整合素谱,并影响MEC与细胞外基质之间的相互作用。特别是,bFGF对胶原/层粘连蛋白受体α2β1的上调可能为活化的内皮细胞提供更强的能力,使其能够穿过其下方的基底膜和间质基质进行迁移。