| MAPK相互作用蛋白激酶1对心肌细胞炎症的作用 |
| 投稿时间：2017-06-14 修订日期：2017-06-20 点此下载全文 |
| 引用本文：袁园,车妍,王兆鹏,靳亚阁,唐其柱.MAPK相互作用蛋白激酶1对心肌细胞炎症的作用[J].医学研究杂志,2018,47(3):62-66 |
| DOI：
10.11969/j.issn.1673-548X.2018.03.016 |
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| 基金项目:湖北省医学领军人才培养工程专项基金资助项目；中央高校基本科研业务费专项基金资助项目（2042016kf0119） |
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| 中文摘要:目的 于在体水平和离体水平研究MAPK相互作用蛋白激酶1对心肌细胞炎症的作用。方法 应用MAPK相互作用蛋白激酶1基因敲除小鼠和C57 BL/6野生型小鼠，行主动脉缩窄术，于术后4周取材。应用免疫荧光染色，检测心肌组织中P-NF-κBp65在心肌细胞中的核转位。应用Western blot法检测心肌组织中P-NF-κBp65和TNF-α。应用Mnk1 shRNA腺病毒转染技术，降低H9c2细胞中Mnk1的表达，给予血管紧张素Ⅱ刺激48h。应用免疫荧光染色，检测H9c2细胞中P-NF-κBp65的核转位。应用RT-PCR检测H9c2细胞中TNF-α mRNA的表达。结果 在体实验表明，主动脉缩窄术后4周，与野生型小鼠相比，MAPK相互作用蛋白激酶1基因敲除小鼠心肌组织中P-NF-κBp65在心肌细胞中的核转位明显增多，TNF-α和P-NF-κBp65的蛋白表达明显增加。离体实验表明，MAPK相互作用蛋白激酶1表达降低的H9c2细胞中P-NF-κBp65的核转位明显增多，TNF-α mRNA的表达明显增加。结论 MAPK相互作用蛋白激酶1基因缺失促进压力负荷诱导的小鼠心肌组织炎症，其表达降低可促进血管紧张素Ⅱ诱导的心肌细胞炎症。 |
| 中文关键词:MAPK相互作用蛋白激酶1 炎症 心肌细胞 |
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| Effect of MAP Kinase-interacting Kinase 1 on Myocardial Inflammation |
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| Abstract:Objective To investigate the effect of MAP kinase-interacting kinase 1 (Mnk1) on myocardial inflammation. Methods Using Mnk1 gene knockout mice and C57 BL/6 wild type mice, we investigated the nuclear localization of NF-κBp65 and the protein levels of P-NF-κBp65 and TNF-α in heart tissue after 4 weeks of aortic banding by immunofluorescence and Western blot respectively. For the in vitro studies, the expression of Mnk1 in H9c2 cells was knocked down using adenovirus expressing Mnk1 shRNA. And the cells (control group and Mnk1 shRNA group) were stimulated with angiotensin Ⅱ for 48 hours. The nuclear localization of NF-κBp65 and the mRNA level of TNF-α was analyzed by immunofluorescence and RT-PCR respectively. Results The in vivo studies showed that P-NF-κBp65 nuclear translocation significantly increased in the heart tissue of Mnk1 gene knockout mice as compared with C57 BL/6 wild type mice. Furthermore, the protein levels of P-NF-κBp65 and TNFα increased as mediated by pressure overload, especially in the Mnk1 gene knockout mice. The in vitro studies indicated that decreased Mnk1 expression increased P-NF-κBp65 nuclear translocation and TNF-α mRNA expression in angiotensin Ⅱ-stimulated H9c2 cells. Conclusion Mnk1 gene knockout accelerate pressure overload-induced Ⅱ myocardial inflammation, decreased Mnk1 expression led to more aggressive cardiomyocyte inflammation induced by angiotensin. |
| keywords:MAP kinase-interacting kinase 1 Inflammation Cardiomyocytes |
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