中文摘要：

目的探讨切应力与血管平滑肌细胞（VSMCs）对内皮细胞（ECs）增殖功能的影响及其一些分子机制。方法应用平行平板流动腔系统对单独培养的ECs以及与VSMCs联合培养的ECs施加15dyn/cm2（1dyn=10-5N）的正常切应力;Western blot技术检测反映细胞增殖能力的分子—增殖细胞核抗原（PCNA）的表达及细胞内信号转导分子Akt的磷酸化水平。静态条件下,以单独培养ECs为对照组,将ECs与VSMCs隔开培养,并应用TGFβ1封闭性抗体,观察TGFβ1在VSMCs诱导ECs增殖中的作用。结果正常切应力抑制了ECs增殖及p-Akt表达,VSMCs在与ECs联合培养及隔开培养时均明显促进ECs增殖及p-Akt表达。正常切应力部分逆转了联合培养VSMCs诱导的ECs增殖和p-Akt表达,而TGFβ1封闭性抗体能够拮抗隔开培养VSMCs诱导的ECs增殖和p-Akt表达。结论正常切应力可视为血管的保护因子,抑制ECs增殖;VSMCs通过旁分泌作用诱导了ECs增殖;TGFβ1及PI3/Akt信号分子参与了其调节过程。

英文摘要：

Objective To investigate the effects of shear stress and vascular smooth muscle cells（VSMCs） on the proliferation of endothelial cells（ECs） and the molecular mechanism involved in.Method Using parallelplate flow chamber system,normal shear stress of 15 dyn/cm2（1 dyn =10-5 N） was applied to ECs cultured singly and co-cultured with VSMCs respectively.Then,the expression of PCNA,a molecule representing cell proliferation ability,and phosphorylation of Akt were analyzed by Western blotting in order to investigate the roles of shear stress and VSMCs in EC proliferation.Under the static condition,the expressions of PCNA and p-Akt were analyzed in ECs co-cultured with VSMCs with and without physical contact.And then TGFβ1 neutralizing antibody was employed to demonstrate the contribution of TGFβ1 in VSMCs induced EC proliferation.Results Normal shear stress decreased EC proliferation and Akt phosphorylation.VSMCs increased EC proliferation and Akt phosphorylation in both co-culture conditions with and without physical contact.Normal shear stress partly reversed the increase of proliferation and Akt phosphorylation in ECs with physical contact to VSMCs,and TGFβ1 neutralizing antibody exerted the similar effects in ECs without physical contact to VSMCs.Conclusions Normal shear stress is a protective factor with its inhibitory effect on EC proliferation.VSMCs induced EC proliferation via TGFβ1 and p-Akt pathways by paracrine model.