Journal
CELLULAR & MOLECULAR BIOLOGY LETTERS
Volume 24, Issue 1, Pages -Publisher
BMC
DOI: 10.1186/s11658-019-0187-4
Keywords
Myocardial infarction; Hypoxia-induced injury; miR-30b-5p; Aven
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Funding
- Chinese National Natural Science Foundation [82013014]
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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.
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