首页> 外文期刊>Endothelium: Journal of endothelial cell research >Cyclic stretch induces the expression of vascular endothelial growth factor in vascular smooth muscle cells.
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Cyclic stretch induces the expression of vascular endothelial growth factor in vascular smooth muscle cells.

机译:循环拉伸诱导血管平滑肌细胞中血管内皮生长因子的表达。

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OBJECTIVE: Accumulating evidence links the release of vascular endothelial growth factor (VEGF) by vascular smooth muscle cells (VSMC) to normal endothelial cell (EC) function, repair and maintenance. Using an in vitro model we investigate the role of cyclic stretch on both the release of VEGF by VSMC and the phosphorylation of a VEGF receptor on EC. METHODS: Bovine VSMC and EC were exposed to 10% cyclic strain for 4 hours. VEGF mRNA steady-state levels of VSMC were analysed by northern blot hybridisation. The presence of secreted VEGF from VSMC was determined by assaying the migration of EC. VEGF receptor phosphorylation on stretched EC was assayed by immunoblotting. RESULTS: The steady-state level of VEGF mRNA in stretched VSMC increased 3.3 (+/- 0.6) fold above that of unstretched VSMC (p < 0.005). Migration of EC was stimulated 8.3 (+/- 1.1) and 14.6 (+/- 1.3) fold by media from unstretched and stretched VSMC respectively, demonstrating a 1.8 fold increase due to stretch alone (p < 0.05). Cyclic stretch resulted in phosphorylation of the VEGF receptor KDR. CONCLUSION: Exposure of VSMC to physiological levels of stretch induces a biologically significant increase in VEGF secretion and may provide an arterial stimulus for maintenance of steady state levels of VEGF essential for EC survival.
机译:目的:越来越多的证据表明血管平滑肌细胞(VSMC)释放血管内皮生长因子(VEGF)与正常内皮细胞(EC)的功能,修复和维持有关。使用体外模型,我们研究了循环拉伸对VSMC释放VEGF以及EC上VEGF受体磷酸化的作用。方法:将牛VSMC和EC暴露于10%循环应变4小时。通过northern印迹杂交分析VSMC的VEGF mRNA稳态水平。通过测定EC的迁移来确定从VSMC分泌的VEGF的存在。通过免疫印迹测定拉伸的EC上的VEGF受体磷酸化。结果:拉伸的VSMC中VEGF mRNA的稳态水平比未拉伸的VSMC升高了3.3倍(+/- 0.6)倍(p <0.005)。来自未拉伸和拉伸的VSMC的培养基分别刺激EC迁移8.3(+/- 1.1)和14.6(+/- 1.3)倍,这表明单独拉伸所导致的EC迁移增加了1.8倍(p <0.05)。循环拉伸导致VEGF受体KDR的磷酸化。结论:将VSMC暴露于生理水平的拉伸可诱导VEGF分泌的生物学显着增加,并可为维持EC生存所必需的稳态VEGF水平提供动脉刺激。

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