血管紧张素 II 通过血管紧张素受体 1 依赖性途径诱导载脂蛋白 E 基因敲除小鼠主动脉粥样硬化斑块中细胞外基质金属蛋白酶诱导剂的表达。
Angiotensin II induces extracellular matrix metalloproteinase inducer expression via an AT1R dependent pathway in aortic atherosclerotic plaque in apolipoprotein E knockout mice.
机构信息
Department of Cardiology, Kunming General Hospital of Chengdu Military Area, Yunnan, China.
出版信息
J Renin Angiotensin Aldosterone Syst. 2012 Mar;13(1):67-75. doi: 10.1177/1470320311423780. Epub 2011 Oct 21.
UNLABELLED
The pathogenesis of acute coronary syndrome is rupture of vulnerable plaque. Extracellular matrix metalloproteinase inducer (EMMPRIN) is reported to have a important role in the destabilization of atheroma.
OBJECTIVES
this investigation examined the effect of angiotensin II (Ang II) on EMMPRIN expression in atherosclerotic plaques in ApoE knockout mice.
METHODS
ApoE knockout mice were fed a high fat diet to establish an atherosclerosis model then intervention was made with Ang II and valsartan. EMMPRIN gene and its protein expression were measured by real-time PCR immunohistochemistry, and Western blot.
RESULTS
EMMPRIN gene and protein expression intervened with Ang II were significantly increased; valsartan could inhibit the effect of Ang II.
CONCLUSION
Ang II up-regulated EMMPRIN expression in atherosclerotic plaque via AT1R, and valsartan could inhibit the effect of Ang II.
目的
本研究旨在探讨血管紧张素 II（Ang II）对载脂蛋白 E 基因敲除（ApoE-/-）小鼠动脉粥样硬化斑块中细胞外基质金属蛋白酶诱导因子（EMMPRIN）表达的影响。
方法
采用高脂饮食喂养 ApoE-/-小鼠建立动脉粥样硬化模型，然后用 Ang II 和缬沙坦进行干预。通过实时 PCR、免疫组织化学和 Western blot 检测 EMMPRIN 基因及其蛋白的表达。
结果
Ang II 干预组的 EMMPRIN 基因和蛋白表达明显增加；缬沙坦可抑制 Ang II 的作用。
结论
Ang II 通过 AT1R 上调动脉粥样硬化斑块中的 EMMPRIN 表达，而缬沙坦可抑制 Ang II 的作用。
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