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学科主题基础医学
miR-499 protects cardiomyocytes from H2O2-induced apoptosis via its effects on Pdcd4 and Pacs2
Wang, Jiaji1; Jia, Zhuqing1; Zhang, Chenguang1; Sun, Min2; Wang, Weiping1; Chen, Ping1; Ma, Kangtao1; Zhang, Youyi3; Li, Xianhui1; Zhou, Chunyan1
关键词miR-499 PDCD4 PACS2 BID c-Jun mitochondrial apoptosis pathway
刊名RNA BIOLOGY
2014-04-01
DOI10.4161/rna.28300
11期:4页:339-350
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology
研究领域[WOS]Biochemistry & Molecular Biology
关键词[WOS]ACUTE MYOCARDIAL-INFARCTION ; N-TERMINAL KINASE ; HEART-FAILURE ; MICRORNA EXPRESSION ; OXIDATIVE STRESS ; SUPPRESSOR PDCD4 ; GENE ONTOLOGY ; CASPASE 8 ; CELLS ; PROLIFERATION
英文摘要

Background: microRNAs (miRNAs) are a class of small, non-coding endogenous RNAs that post-transcriptionally regulate some protein-coding genes. miRNAs play an important role in many cardiac pathophysiological processes, including myocardial infarction, cardiac hypertrophy, and heart failure. miR-499, specifically expressed in skeletal muscle and cardiac cells, is differentially regulated and functions in heart development. However, the function of miR-499 in mature heart is poorly understood.

Results: We report that cardiac-abundant miR-499 could protect neonatal rat cardiomyocytes against H2O2-induced apoptosis. Increased miR-499 level favored survival, while decreased miR-499 level favored apoptosis. We identified three proapoptotic protein-coding genes-Pdcd4, Pacs2, and Dyrk2-as targets of miR-499. miR-499 inhibited cardiomyocyte apoptosis through its suppressive effect on Pdcd4 and Pacs2 expression, thereby blocking Bid expression and BID mitochondrial translocation. We also found that H2O2-induced phosphorylation of c-Jun transcriptionally upregulated miR-499 expression via binding of phosphorylated c-Jun to the Myh7b promoter.

Conclusions: Our results revealed that miR-499 played an inhibiting role in the mitochondrial apoptosis pathway, and had protective effects against H2O2-induced injury in cardiomyocytes.

语种英语
WOS记录号WOS:000336144900008
项目编号81070112 ; 81071675 ; 81371889 ; 81370236 ; 5122021 ; B07001
资助机构National Natural Science Foundation of China ; Natural Science Foundation of Beijing, China ; Leading Academic Discipline Project of Beijing Education Bureau ; 111 Project of China
引用统计
被引频次:46[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/64693
专题北京大学基础医学院
北京大学药学院_药学院
作者单位1.Peking Univ, Dept Biochem & Mol Biol, Sch Basic Med Sci, Key Lab Mol Cardiovasc Sci,Minist Educ China, Beijing 100871, Peoples R China
2.Peking Univ, Dept Cardiol, Hosp 3, Beijing 100871, Peoples R China
3.Peking Univ, Inst Vasc Med, Hosp 3, Key Lab Mol Cardiovasc Sci,Minist Educ China, Beijing 100871, Peoples R China
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GB/T 7714
Wang, Jiaji,Jia, Zhuqing,Zhang, Chenguang,et al. miR-499 protects cardiomyocytes from H2O2-induced apoptosis via its effects on Pdcd4 and Pacs2[J]. RNA BIOLOGY,2014,11(4):339-350.
APA Wang, Jiaji.,Jia, Zhuqing.,Zhang, Chenguang.,Sun, Min.,Wang, Weiping.,...&Zhou, Chunyan.(2014).miR-499 protects cardiomyocytes from H2O2-induced apoptosis via its effects on Pdcd4 and Pacs2.RNA BIOLOGY,11(4),339-350.
MLA Wang, Jiaji,et al."miR-499 protects cardiomyocytes from H2O2-induced apoptosis via its effects on Pdcd4 and Pacs2".RNA BIOLOGY 11.4(2014):339-350.
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