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Down-regulation of miR-30b-5p protects cardiomyocytes against hypoxia-induced injury by targeting Aven

BACKGROUND: Ischemia/hypoxia-induced cardiomyocyte apoptosis has been considered as a main cause of myocardial infarction. Here, we aimed to investigate the functional role of miR-30b-5p in hypoxic cardiomyocytes. METHODS: AC16 human cardiomyocytes were cultured under hypoxia to simulate myocardial...

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Detalles Bibliográficos
Autores principales: Zhang, Lanfang, Jia, Xinwei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6873433/
https://www.ncbi.nlm.nih.gov/pubmed/31768184
http://dx.doi.org/10.1186/s11658-019-0187-4
Descripción
Sumario:BACKGROUND: Ischemia/hypoxia-induced cardiomyocyte apoptosis has been considered as a main cause of myocardial infarction. Here, we aimed to investigate the functional role of miR-30b-5p in hypoxic cardiomyocytes. METHODS: AC16 human cardiomyocytes were cultured under hypoxia to simulate myocardial infarction. A qRT-PCR assay was performed to determine miR-30b-5p expression in hypoxic cardiomyocytes. Cell survival, injury and apoptosis were assessed by MTT, lactate dehydrogenase (LDH) release, and flow cytometry assays, respectively. The target gene of miR-30b-5p in hypoxic cardiomyocytes was validated by luciferase reporter assay and Western blotting. RESULTS: MiR-30b-5p expression was found to be significantly upregulated in hypoxic AC16 cells. The in vitro experiments showed that downregulation of miR-30b-5p effectively alleviated hypoxia-induced cardiomyocyte injury. Furthermore, Aven is a potential target gene of miR-30b-5p and its downregulation could partially reverse the influence of miR-30b-5p knockdown on AC16 cells under hypoxia. CONCLUSIONS: Inhibition of miR-30b-5p could protect cardiomyocytes against hypoxia-induced injury by targeting Aven.