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MicroRNA-133b Alleviates Hypoxia Injury by Direct Targeting on NOD-Like Receptor Protein 3 in Rat H9c2 Cardiomyocyte

OBJECTIVE: MiR-133b was dysregulated in myocardial infarction. However, the role and mechanism of miR-133b in myocardial infarction remains unclear. This study was aimed to explore the role of miR-133b in H9c2 cell injury induced by hypoxia and to investigate the underlying molecular mechanism. METH...

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Detalles Bibliográficos
Autores principales: Zhou, Yongmei, Huang, Hui, Hou, Xiaolin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6925740/
https://www.ncbi.nlm.nih.gov/pubmed/31885905
http://dx.doi.org/10.1155/2019/8092461
Descripción
Sumario:OBJECTIVE: MiR-133b was dysregulated in myocardial infarction. However, the role and mechanism of miR-133b in myocardial infarction remains unclear. This study was aimed to explore the role of miR-133b in H9c2 cell injury induced by hypoxia and to investigate the underlying molecular mechanism. METHODS: Cell injury was assessed by cell viability, migration, invasion, and apoptosis assays. The expression of miR-133b and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) mRNA was determined by qRT-PCR. The levels of apoptosis-related proteins and NLRP3 were detected by western blotting. RESULTS: Results showed that hypoxia significantly reduced cell viability, migration, and invasion, but increased apoptosis of H9c2 cells. Downregulation of miR-133b aggravated the cell injury induced by hypoxia. MiR-133b was directly targeted on NLRP3. Overexpression of NLRP3 significantly inhibited cell viability, migration, and invasion but induced cell apoptosis in H9c2 treated with hypoxia. CONCLUSIONS: Thus, miR-133b protects H9c2 against hypoxia injury via downregulation of NLRP3.