MicroRNA-1 facilitates hypoxia-induced injury by targeting NOTCH3.
J Cell Biochem
; 121(11): 4458-4469, 2020 11.
Article
em En
| MEDLINE
| ID: mdl-32030815
ABSTRACT
Cell proliferation, apoptosis, and autophagy have been reported to be related to myocardial ischemia injury. MicroRNAs have attracted wide attention on regulating cell proliferation, apoptosis, and autophagy. miR-1 expression has been reported to be dysregulated in cardiac tissue or cells with hypoxia, while the exact roles as well as underlying mechanism remain poorly understood. In this study, we investigated the potential roles of miR-1 in cell proliferation, apoptosis, and autophagy in hypoxia-treated cardiac injury and explored the underlying mechanism using H9c2 cells. Results showed that hypoxic stimulation inhibited cell proliferation and the expression of miR-1 but promoted cell apoptosis in H9c2 cells. Moreover, overexpression of miR-1 promoted cell apoptosis and inhibited cell proliferation and autophagy in H9c2 cells treated with hypoxia, while its knockdown played an opposite effect. In addition, bioinformatics, luciferase reporter, and RNA immunoprecipitation analyses indicated that NOTCH3 was a direct target of miR-1 and its upregulation reversed the effects of miR-1 on cell proliferation, apoptosis, and autophagy in hypoxia-treated H9c2 cells. Taken together, our data suggested that miR-1 promoted hypoxia-induced injury by targeting NOTCH3, indicating novel therapeutic targets for treatment of myocardial ischemia injury.
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Base de dados:
MEDLINE
Assunto principal:
Biomarcadores
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Traumatismo por Reperfusão Miocárdica
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Regulação da Expressão Gênica
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Miócitos Cardíacos
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MicroRNAs
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Receptor Notch3
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Hipóxia
Idioma:
En
Ano de publicação:
2020
Tipo de documento:
Article