期刊
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
卷 51, 期 2, 页码 778-792出版社
KARGER
DOI: 10.1159/000495332
关键词
Selenium Deficiency; Myocardiosis; miR-2954; Autophagy; Apoptosis; PI3K
资金
- National Natural Science Foundation of China [31872531]
- Open Projects of Key Laboratory of Animal Cellular and Genetic Engineering of Heilongjiang Province [KF201703]
- Merit-based Funding for Returned Oversea Student of Heilongjiang Province [2018QD0005]
- Foundation for Young Talents in Higher Education of Heilongjiang, China [UNPYSCT-2015009]
- Academic backbone Project of Northeast Agricultural University [17XG11]
Background/Aims: Selenium (Se) deficiency can lead to several cardiac diseases, including Keshan disease in humans, mulberry heart disease in pigs and cardiac injury in chickens. MicroRNAs have been a research focus in recent years and have been shown to participate in a new avenue of cell death-autophagy, which can play a significant role in several types of heart disease. Methods: MicroRNAome analysis showed that the expression of miR-2954 was increased in the myocardium of selenium-deficient chickens, and PI3K was predicted to be the target gene. The target relationship between miR-2954 and PI3K was verified with a double fluorescence enzyme assay and RNA Protein Interaction Prediction and molecular docking software. qRT-PCR and western blotting were used to detect the expression of PI3K and related pathway components in selenium-deficient chickens and miR-2954 knockout/overexpression cardiomyocytes. Results: In this study, we observed that miR-2954 overexpression led to inhibition of PI3K pathway in vivo and in vitroled to inhibition of the PI3K pathway in vivo and in vitro. Conclusion: The expression of miR-2954 was increased in selenium-deficient myocardium, whereas overexpression of miR-2954 led to autophagy and apoptosis of myocardial cells during cardiac injury through regulation of the PI3K pathway; whether this phenomenon is a self-protection mechanism of the organism or damage caused by miR-2954 requires further study. Our findings provides new insight apoptosis in cardiomyocytes; additionally, we aim to provide a new direction for the diagnosis and targeted treatment of myocardial diseases.
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