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LncRNA 0003250 accelerates heart autophagy and binds to miR‐17‐5p as a competitive endogenous RNA in chicken induced by selenium deficiency
Author(s) -
Yang Jie,
Shi Guangliang,
Gong Yafan,
Cai Jingzeng,
Zheng Yingying,
Zhang Ziwei
Publication year - 2021
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29831
Subject(s) - autophagy , microrna , downregulation and upregulation , long non coding rna , transcriptome , microbiology and biotechnology , rna , in vitro , endogeny , messenger rna , biology , in vivo , competing endogenous rna , small nucleolar rna , programmed cell death , gene expression , gene , genetics , biochemistry , apoptosis
Abstract Long noncoding RNAs (LncRNAs) have been demonstrated to be associated with a variety of myocardial diseases, but how LncRNAs regulate autophagy in selenium (Se)‐deficient myocardial injury is infrequently reported. Here, we screened out a novel long noncoding RNA, microRNA, and ATG7 through transcriptomic results. We employed a Se‐deficient chicken model in vivo, and primary cultured cardiomyocytes treated by correlation in vitro. The results showed that Se deficiency upregulated the expression of ATG7, and miR‐17‐5p inhibited cardiomyocyte autophagy by targeting ATG7. Furthermore, we found that LncRNA 0003250 regulated miR‐17‐5p, and thus affected the expression of ATG7 and autophagic cell death. Our present study proposed a novel model for the regulation of cardiomyocytes autophagy, which includes LncRNA 0003250, miR‐17‐5p and ATG7 in the chicken heart. Our conclusions may provide a feasible diagnostic tool for Se‐deficient cardiomyocyte injury.