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首页> 外文期刊>Journal of Cellular Physiology >Tenascin-C enhances crosstalk signaling of integrin alphavbeta3/PDGFR-beta complex by SRC recruitment promoting PDGF-induced proliferation and migration in smooth muscle cells.
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Tenascin-C enhances crosstalk signaling of integrin alphavbeta3/PDGFR-beta complex by SRC recruitment promoting PDGF-induced proliferation and migration in smooth muscle cells.

机译：Tenascin-C提高串扰信号整合素alphavbeta3 SRC / PDGFR-beta复杂招聘促进PDGF-induced扩散并在平滑肌细胞迁移。

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摘要

Migration and proliferation of smooth muscle cells (SMCs) are key events during neointimal formation in pathological conditions of vessels. Tenascin-C (TNC) is upregulated in the developing neointima of lesions. We evaluated the effects of TNC on responses of SMCs against platelet-derived growth factor (PDGF) stimulation. TNC coated on substrate promoted PDGF-BB-induced proliferation and migration of rat SMC cell line A10 in BrdU incorporation and transwell assays, respectively. Immunoblotting showed that TNC substrate enhanced autophosphorylation of PDGFR-beta after PDGF-BB stimulation. Integrin alphavbeta3 is known to be a receptor for TNC in SMCs. In immunofluorescence and immunoblot of integrin alphav subunit, clustering of alphav-positive focal adhesions and upregulated alphav expression were observed in the cells on TNC substrate. Immunoprecipitation using anti-integrin alphavbeta3 antibody demonstrated that PDGFR-beta and integrin alphavbeta3 were co-precipitated and that the relative amount of PDGFR-beta after the stimulation was increased by TNC treatment. TNC also promoted phosphorylation of focal adhesion kinase (FAK) at tyrosine (Y) 397 and Y925. The phosphorylated FAK was localized at focal adhesions in immunofluorescence. Phosphorylated SRC at Y418 was also seen at focal adhesions. Immunoprecipitation with alphav antibody showed increased SRC association with the integrin signaling complex in the cells on TNC after PDGF treatment. In the cells on TNC substrate, crosstalk signaling between integrin alphavbeta3 and PDGFR-beta could be amplified by SRC and FAK recruited to focal adhesions, followed by enhanced proliferation and migration of A10 cells by PDGF-BB.
机译：平滑肌细胞的迁移和增殖(smc)是关键事件在新生内膜的形成在病理条件下的血管。(TNC)是调节在发展中neointima的病变。对血小板源生长的smc的反应因子(PDGF)刺激。衬底提升PDGF-BB-induced扩散和迁移的老鼠SMC细胞系A10 BrdU分别掺入和transwell化验。免疫印迹显示过渡委员会基质增强的自身磷酸化PDGFR-beta PDGF-BB之后刺激。过渡委员会在smc的受体。和免疫印迹的整合素alphav亚基,集群alphav-positive焦粘连和调节alphav表达式被观察到过渡委员会衬底上的细胞。使用anti-integrin alphavbeta3抗体证明PDGFR-beta和整合素alphavbeta3共沉淀的PDGFR-beta后的相对数量刺激增加了过渡委员会处理。也促进了粘着斑的磷酸化在酪氨酸激酶(FAK) 397和Y925 (Y)。磷酸化FAK在病灶局部在免疫荧光粘连。SRC Y418也见过焦粘连。免疫沉淀反应与alphav抗体显示SRC与整合素增加信号的复杂细胞PDGF后过渡委员会治疗。整合素alphavbeta3之间的串扰信号SRC和FAK和PDGFR-beta可能被放大招募焦粘连,紧随其后增强A10细胞的增殖和迁移PDGF-BB。

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