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Platelet-derived growth factor modulates rat vascular smooth muscle cell responses on laminin-5 via mitogen-activated protein kinase-sensitive pathways

机译:血小板衍生的生长因子通过促分裂原激活的蛋白激酶敏感途径调节层粘连蛋白5对大鼠血管平滑肌细胞的反应

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摘要

BackgroundA treatment to remove vascular blockages, angioplasty, can cause damage to the vessel wall and a subsequent abnormal wound healing response, known as restenosis. Vascular smooth muscle cells (VSMC) lining the vessel wall respond to growth factors and other stimuli released by injured cells. However, the extracellular matrix (ECM) may differentially modulate VSMC responses to these growth factors, such as proliferation, migration and adhesion. Our previous reports of low-level expression of one ECM molecule, laminin-5, in normal and injured vessels suggest that laminin-5, in addition to growth factors, may mediate VSMC response following vascular injury. To elucidate VSMC response on laminin-5 we investigated-the role of platelet-derived growth factor (PDGF-BB) in activating the mitogen-activated protein kinase (MAPK) signaling cascade as a possible link between growth-factor initiated phenotypic changes in vitro and the ECM.
机译:背景去除血管阻塞,血管成形术的治疗可能会损坏血管壁,并导致随后的异常伤口愈合反应,称为再狭窄。血管壁内壁的血管平滑肌细胞(VSMC)对受伤细胞释放的生长因子和其他刺激作出反应。但是,细胞外基质(ECM)可能会差异调节VSMC对这些生长因子的反应,例如增殖,迁移和粘附。我们先前关于正常血管和受伤血管中一种ECM分子层粘连蛋白5的低水平表达的报道表明,层粘连蛋白5除生长因子外,还可以介导血管损伤后的VSMC反应。为了阐明层粘连蛋白5上的VSMC反应,我们研究了血小板源性生长因子(PDGF-BB)在激活有丝分裂原激活的蛋白激酶(MAPK)信号级联反应中的作用,作为体外生长因子引发的表型变化之间的可能联系和ECM。

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