Overexpression of microRNA-135b-5p attenuates acute myocardial infarction injury through its anti-oxidant and anti-apptotic properties
Yanyan Liu1
Yahan Yu2
Xinyao Wang2
Guanqun Liu2
Xinda Yin2
Yunlong Bai3
Zhimin Du1
1.Zhuhai People's Hospital,Guangdong Provincial Key Laboratory of Tumor Interventional Diagnosis and Treatment,Zhuhai Hospital Affiliated With Jinan University,Jinan University,Zhuhai 519000,China;Department of Pharmacology(State-Province Key Laboratories of Biomedicine-Pharmaceutics of China,Key Laboratory of Cardiovascular Medicine Research,Ministry of Education),College of Pharmacy,Harbin Medical University,Harbin 150081,China2.Department of Pharmacology(State-Province Key Laboratories of Biomedicine-Pharmaceutics of China,Key Laboratory of Cardiovascular Medicine Research,Ministry of Education),College of Pharmacy,Harbin Medical University,Harbin 150081,China;Translational Medicine Research and Cooperation Center of Northern China,Heilongjiang Academy of Medical Sciences,Harbin 150081,China3.Department of Pharmacology(State-Province Key Laboratories of Biomedicine-Pharmaceutics of China,Key Laboratory of Cardiovascular Medicine Research,Ministry of Education),College of Pharmacy,Harbin Medical University,Harbin 150081,China;Translational Medicine Research and Cooperation Center of Northern China,Heilongjiang Academy of Medical Sciences,Harbin 150081,China;Joint International Research Laboratory of Cardiovascular Medicine,Ministry of Education,College of Pharmacy,Harbin Medical University,Harbin 150081,China
摘要：Objective: Myocardial infarction (MI) remains the leading cause of morbidity and mortality due partly to the limited regenerative capacity of cardiomyocytes to replace cardiomyocyte lost due to apoptosis. Inhibiting cardiomyocyte apoptosis is recognized as an effective therapeutic approach for MI. MicroRNAs (miRNAs, miRs), which regulate target genes at the post-transcriptional level, play a significant role in the regulation of cardiovascular diseases such as MI. MicroRNA-135b (miR-135b) has a protective effect on cardiomyocytes. However, the role of miR-135b in cardiomyocyte apoptosis in infarct myocardium needs further clarification. Methods: We generated α-MHC-miR-135b transgenic mice to investigate the role of miR-135b in myocardial injury after MI. MiR-135b mimic and negative control (NC) were transfected into H2O2-induced cardiomyocytes to evaluate the effect of overexpression of miR-135b on the levels of reactive oxygen species (ROS) and apoptosis. Results: Our results showed that overexpression of miR-135b had protective effect on cardiomyocyte injury both in vivo and in vitro. MiR-135b inhibited cardiomyocyte apoptosis and ROS generation, downregulated pro-apoptosis proteins (cleaved-caspase-3 and Bax), and increased anti-apoptosis protein (Bcl-2). Moreover, miR-135b showed an inhibitory effect on apoptosis-related protein target transient receptor potential vanilloid-type 4 (TRPV4) cation channel. Conclusion: MiR-135b might be considered a new molecular target for potential replacement therapy as antiapoptotic cardioprotection in the setting of MI.
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论文发表日期：2021-04-30
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：10( 85-94 )
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