Li Z, Alavi M Z, Moore S
Department of Pathology, McGill University, Montreal, Canada.
Int J Exp Pathol. 1994 Jun;75(3):169-77.
Endothelial denudation of rabbit aorta induces smooth muscle cell (SMC) migration and proliferation, resulting in a thickened neointima, showing features in common with atherosclerotic lesions. The SMC proliferation has been reported as a transient healing process, which regresses when the neointima is covered by regenerated endothelium. In this study, we examined the cellular proliferation of neointimal SMC, derived from denuded and from re-endothelialized areas of aortic explants. The results show that the neointimal SMC retain a higher rate of proliferation, even 15 weeks after a single endothelial injury by a balloon catheter. Neointimal SMC release more PDGF-AB and TGF-beta 1, which may play a mitogenic role for SMC proliferation. The data demonstrating that injury-induced stimulation of neointimal SMC proliferation is a persistent process, emphasize the importance of injury mechanisms of atherogenesis.
兔主动脉内皮剥脱可诱导平滑肌细胞（SMC）迁移和增殖，导致新生内膜增厚，呈现出与动脉粥样硬化病变相同的特征。据报道，SMC增殖是一个短暂的愈合过程，当新生内膜被再生的内皮覆盖时，该过程会消退。在本研究中，我们检测了源自主动脉外植体剥脱区域和再内皮化区域的新生内膜SMC的细胞增殖情况。结果显示，即使在通过球囊导管进行单次内皮损伤15周后，新生内膜SMC仍保持较高的增殖率。新生内膜SMC释放更多的血小板源性生长因子-AB（PDGF-AB）和转化生长因子-β1（TGF-β1），这可能对SMC增殖起促有丝分裂作用。这些数据表明，损伤诱导的新生内膜SMC增殖刺激是一个持续的过程，强调了动脉粥样硬化发生损伤机制的重要性。
