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MST1-Hippo pathway regulates inflammation response following myocardial infarction through inhibiting HO-1 signaling pathway
Journal of Receptors and Signal Transduction ( IF 2.8 ) Pub Date : 2020-02-13 , DOI: 10.1080/10799893.2020.1726954 Yanan Tian 1 , Haijiu Song 2 , Dapeng Jin 1 , Na Hu 1 , Lixian Sun 1
Journal of Receptors and Signal Transduction ( IF 2.8 ) Pub Date : 2020-02-13 , DOI: 10.1080/10799893.2020.1726954 Yanan Tian 1 , Haijiu Song 2 , Dapeng Jin 1 , Na Hu 1 , Lixian Sun 1
Affiliation
Abstract Context: Mammalian STE20-like protein kinases 1 (MST1) has been found to be associated with cardiomyocyte damage following acute myocardial infarction. Aim: The aim of our study is to explore the influence of MST1 in inflammation response following myocardial infarction. Methods: Cardiomyocyte cell line was used in vitro with hypoxia treatment to establish myocardial infarction model. ELISA, qPCR, Western blots, and siRNA technology were used to analyze the role of MST1 in inflammation response following myocardial infarction. Results: The transcription and expression of MST1 was significantly elevated following myocardial infarction. Loss of MST1 attenuated the levels of inflammation response and thus contributed to the survival of cardiomyocyte in vitro. Mechanistically, MST1 deletion reversed the activity of heme oxygenase-1 (HO-1) and thus reduced hypoxia-mediated cardiomyocyte death. Conclusions: Altogether, in this study, we found that MST1-Hippo pathway is activated in myocardial infarction and contributes to the inflammation response in cardiomyocytes through inhibiting the HO-1 signaling pathway. This finding would provide a potential target to reverse cardiomyocyte viability and reduce inflammation response in myocardial infarction.
中文翻译:
MST1-Hippo通路通过抑制HO-1信号通路调节心肌梗死后的炎症反应
摘要背景:已发现哺乳动物 STE20 样蛋白激酶 1 (MST1) 与急性心肌梗死后的心肌细胞损伤有关。目的:我们研究的目的是探讨 MST1 在心肌梗死后炎症反应中的影响。方法:体外用心肌细胞系低氧处理建立心肌梗死模型。ELISA、qPCR、Western印迹和siRNA技术被用于分析MST1在心肌梗塞后炎症反应中的作用。结果:心肌梗死后MST1的转录和表达显着升高。MST1 的缺失减弱了炎症反应的水平,从而有助于体外心肌细胞的存活。从机制上讲,MST1 缺失逆转了血红素加氧酶-1 (HO-1) 的活性,从而减少了缺氧介导的心肌细胞死亡。结论:总之,在本研究中,我们发现 MST1-Hippo 通路在心肌梗死中被激活,并通过抑制 HO-1 信号通路促进心肌细胞的炎症反应。这一发现将为逆转心肌细胞活力和减少心肌梗塞的炎症反应提供一个潜在的目标。
更新日期:2020-02-13
中文翻译:
MST1-Hippo通路通过抑制HO-1信号通路调节心肌梗死后的炎症反应
摘要背景:已发现哺乳动物 STE20 样蛋白激酶 1 (MST1) 与急性心肌梗死后的心肌细胞损伤有关。目的:我们研究的目的是探讨 MST1 在心肌梗死后炎症反应中的影响。方法:体外用心肌细胞系低氧处理建立心肌梗死模型。ELISA、qPCR、Western印迹和siRNA技术被用于分析MST1在心肌梗塞后炎症反应中的作用。结果:心肌梗死后MST1的转录和表达显着升高。MST1 的缺失减弱了炎症反应的水平,从而有助于体外心肌细胞的存活。从机制上讲,MST1 缺失逆转了血红素加氧酶-1 (HO-1) 的活性,从而减少了缺氧介导的心肌细胞死亡。结论:总之,在本研究中,我们发现 MST1-Hippo 通路在心肌梗死中被激活,并通过抑制 HO-1 信号通路促进心肌细胞的炎症反应。这一发现将为逆转心肌细胞活力和减少心肌梗塞的炎症反应提供一个潜在的目标。