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首页> 外文期刊>Journal of cellular physiology. >LncRNA 0003250 accelerates heart autophagy and binds to miR-17-5p as a competitive endogenous RNA in chicken induced by selenium deficiency
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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

机译:LncRNA 0003250加速心脏自噬和结合miR-17-5p作为竞争力的内生RNA在硒缺乏引起的鸡

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摘要

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 cardio-myocytes 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 cardio-myocytes 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.
机译:长非编码rna (LncRNAs)证明了与各种有关心肌疾病,但LncRNAs如何调节自噬在硒缺乏心肌(Se)受伤是很少报道。小说长非编码RNA筛选出来,通过转录组和微rna, ATG7结果。体内,主要培养cardio-myocytes治疗相关体外。表明硒缺乏调节表达ATG7, miR-17-5p抑制针对ATG7心肌细胞自噬。此外,我们发现LncRNA 0003250miR-17-5p监管,从而影响了表达ATG7和自噬细胞死亡。本研究提出了一种新的模型cardio-myocytes自噬的调节包括LncRNA 0003250, miR-17-5p ATG7鸡的心。Se-deficient可行的诊断工具心肌细胞损伤。

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