Grosskreutz C L, Anand-Apte B, Dupláa C, Quinn T P, Terman B I, Zetter B, D'Amore P A
Department of Surgery, Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Microvasc Res. 1999 Sep;58(2):128-36. doi: 10.1006/mvre.1999.2171.
Angiogenesis is a complex process that includes recruitment and proliferation of mural cells-smooth muscle cells (SMC) and pericytes. Vascular endothelial growth factor (VEGF) has been shown to play an important role in angiogenesis and is an endothelial cell chemoattractant. In addition, certain VEGF isoforms have been implicated in the normal formation of smooth muscle cell-surrounded arteries. Because VEGF's role as a mural cell chemoattractant had not been explored, we examined the ability of VEGF to influence vascular SMC migration in vitro. A Boyden chamber migration assay demonstrated that VEGF (0-100 ng/ml) caused a dose-dependent migration of SMC. VEGF did not cause proliferation of SMC. Reverse transcriptase-polymerase chain reaction analysis demonstrated the presence of both KDR and flt mRNA, two known VEGF receptors, in SMC cultures. Western blot analysis of SMC lysates confirmed these data, revealing bands migrating at approximately 200 kDa and slightly below 200 kDa consistent with KDR and flt. These observations demonstrate that VEGF receptors are present on SMC, and that VEGF can act as an SMC chemoattractant.
血管生成是一个复杂的过程，包括壁细胞（平滑肌细胞[SMC]和周细胞）的募集和增殖。血管内皮生长因子（VEGF）已被证明在血管生成中起重要作用，并且是一种内皮细胞趋化因子。此外，某些VEGF异构体与平滑肌细胞包绕的动脉的正常形成有关。由于VEGF作为壁细胞趋化因子的作用尚未得到探索，我们研究了VEGF在体外影响血管SMC迁移的能力。博伊登室迁移试验表明，VEGF（0 - 100 ng/ml）引起SMC的剂量依赖性迁移。VEGF不会引起SMC增殖。逆转录聚合酶链反应分析表明，在SMC培养物中存在两种已知的VEGF受体KDR和flt mRNA。对SMC裂解物的蛋白质印迹分析证实了这些数据，显示迁移条带位于约200 kDa和略低于200 kDa处，与KDR和flt一致。这些观察结果表明，SMC上存在VEGF受体，并且VEGF可以作为SMC趋化因子。
