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Knockdown of HIF1A-AS2 suppresses TRIM44 to protect cardiomyocytes against hypoxia-induced injury

文献类型: 外文期刊

作者: Luo, Fang 1 ; Wu, Yitian 3 ; Zhu, Liying 4 ; Zhang, Jun 1 ; Liu, Yixin 1 ; Jia, Weiguo 1 ;

作者机构: 1.Sichuan Univ, West China Hosp, Ctr Gerontol & Geriatr, Chengdu 610041, Sichuan, Peoples R China

2.Sichuan Univ, West China Hosp, Natl Clin Res Ctr Geriatr, Chengdu 610041, Sichuan, Peoples R China

3.Sichuan Univ, West China Hosp, Dept Lab Med, Chengdu 610041, Sichuan, Peoples R China

4.Zhejiang Acad Agr Sci, Inst Plant Protect & Microbiol, State Microbial Technol Zhejiang Prov, Hangzhou 310021, Peoples R China

关键词: HIF1A-AS2; miR-623; myocardial infarction TRIM44

期刊名称:CELL BIOLOGY INTERNATIONAL ( 影响因子:3.612; 五年影响因子:3.055 )

ISSN: 1065-6995

年卷期: 2020 年 44 卷 7 期

页码:

收录情况: SCI

摘要: Myocardial infarction (MI) is a common cardiovascular disease characterized by an interruption of blood and oxygen supply to the heart, which results in gradual damage to the myocardial tissue and ultimately heart failure. The role of long non-coding RNAs in the pathology of MI remains in its infancy, but has been implicated in MI and other heart conditions. For example, the expression of a non-coding RNA hypoxia-inducible factor 1 alpha (HIF1A)-antisense RNA 2 (HIF1A-AS2) has previously been linked to coronary heart disease, however, whether HIF1A-AS2 expression is also high in MI has not been addressed. Here, we report that HIF1A-AS2 is upregulated in hypoxia-treated human cardiomyocytes (HMCs) compared with normal cardiomyocytes, and that silenced HIF1A-AS2 inhibited apoptosis and facilitated viability, migration, and invasion of HMCs. Our data suggested that in MI, HIF1A-AS2 upregulation was associated with miR-623, which promoted expression of tripartite motif containing 44 (TRIM44). Moreover, by upregulating TRIM44 we were able to remedy the HIF1A-AS2 repression of apoptosis in HMCs. Thus, we conclude that cardiomyocytes can be protected against hypoxic-treated injury by knockdown of HIF1A-AS2, which suppresses TRIM44, and that HIF1A-AS2 overexpression is a prognostic indicator of MI.

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