AMPKα2在主动脉夹层形成中的作用及机制
Role and mechanism of AMPKα2 in formation of aortic dissection

雷蕾.AMPKα2在主动脉夹层形成中的作用及机制[J].内科急危重症杂志,2019,25(6):491-495

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DOI：10.11768/nkjwzzzz20190615

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基金项目:湖北省科技厅自然科学基金项目(No:2015CFB072)

作者	单位	E-mail
雷蕾	华中科技大学同济医学院附属同济医院	panyoumin@126.com

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中文摘要:

目的：研究AMPKα2蛋白在主动脉夹层（AD）形成中的作用。方法：通过临床标本收集和体外实验，检测主动脉组织磷酸化AMPKα（Thr172）表达水平、血管平滑肌细胞表型转化、基质金属蛋白酶及炎症通路激活情况。结果：通过临床标本检测，发现AD患者主动脉组织磷酸化AMPKα（Thr172）表达下调，血管平滑肌细胞发生表型转化，基质金属蛋白酶表达上调及炎症通路激活。体外实验采用AMPKα2质粒和相应突变失活型DN-AMPKα2(T172A)质粒转染原代大鼠主动脉血管平滑肌细胞，予以AngⅡ (10 μmol/L)刺激24h，发现过表达AMPKα2可缓解AngⅡ诱导的磷酸化AMPKα（Thr172）下调，减轻血管平滑肌细胞表型转化、基质金属蛋白酶表达及炎症通路激活。而过表达失活型DN-AMPKα2(T172A)加重上述病理改变。结论：AMPKα2促进磷酸化AMPKα(Thr172)表达，缓解主动脉血管平滑肌细胞表型转化、基质金属蛋白酶表达上调及炎症通路激活。

英文摘要:

Objective: To elucidate the role and mechanism of AMPKα2 in the formation of aortic dissection. Methods: The tissue samples were collected from controls and patients with type I aortic dissection, and the expression of phosphorylated-AMPKα (Thr172), phenotypic switch of vascular smooth muscle cells (VSMCs), expression of matrix metalloproteinases (MMPs) and activation of inflammation were detected. Results: Down-regulation of phosphorylated-AMPKα (Thr172), phenotypic switch of VSMCs, up-regulation of MMPs and activation of inflammation were found in human aortic dissection tissues as compared with controls. In vitro, primary rat aortic smooth muscle cells were transfected with AMPKα plasmid or inactive mutant DN-AMPKα2 (T172A) plasmid, incubated with AngII (10μmol/L) for 24h and then subjected to subsequent assays. It was found that the overexpression of AMPKα2 attenuated the down-regulation of phosphorylated-AMPKα (Thr172) and the phenotypic switch of VSMCs, up-regulation of MMPs and activation of inflammation, which were reversely exaggerated by the overexpression of DN-AMPKα (T172A). Conclusion: AMPKα2 up-regulates the expression of phosphorylated-AMPKα (Thr172) and ameliorates the phenotypic switch of VSMCs, up-regulation of MMPs and activation of inflammation.