Key result
Overexpression of miR-490-3p alleviated hypoxia-induced cardiomyocyte injury, apoptosis, and inflammatory responses by directly targeting and downregulating FOXO1.
Why the study?
Although miR-490-3p is downregulated in myocardial tissues of mice with MI, its functions and mechanisms in MI remain unclear.
miR-490-3p alleviates hypoxia-induced cardiomyocyte injury and inflammation by directly targeting FOXO1, suggesting a potential molecular mechanism and therapeutic target for myocardial infarction.
miR-490-3p modulation may protect hypoxic cardiomyocytes; leaves open therapeutic relevance in ischemic heart disease pending in vivo and clinical validation.
BACKGROUND: MicroRNA-490-3p (miR-490-3p) plays a role in the pathogeneses of a variety of cardiovascular diseases. Bioinformatic analysis showed that miR-490-3p was downregulated in the myocardial tissues of mice with myocardial infarction (MI). Nevertheless, the functions and mechanisms of miR-490-3p in MI remain unclear. METHODS: This study used an in-vitro model to investigate the role of miR-490-3p in MI. Human cardiac myocytes (HCMs) were cultured in a hypoxic environment. 3-(4,5)-Dimethylthiahiazo (-zy1)- 3,5-di-phenytetrazoliumromide (MTT) assay and flow cytometry were used to detect cell viability and apoptosis. The expression levels of forkhead box O1 (FOXO1) and miR-490-3p were detected by quantitative real-time PCR and Western blot. The levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), lactate dehydrogenase (LDH), cardiac troponin I (cTnI), and creatine kinase MB (CK-MB) were detected by enzyme-linked immunosorbent assay (ELISA). The targeted relationship between miR-490-3p and FOXO1 3'UTR was determined by a dual-luciferase reporter gene assay. RESULTS: miR-490-3p was significantly down-regulated in hypoxia-induced HCM cells, while FOXO1 was markedly up-regulated. miR-490-3p overexpression inhibited HCM cell inflammatory responses and injury after hypoxia treatment. FOXO1 was validated to be a direct target of miR- 490-3p, and its overexpression weakened the effects of miR-490-3p on cell viability, apoptosis, as well as inflammatory responses. CONCLUSION: miR-490-3p alleviates cardiomyocyte injury via targeting FOXO1 in MI.
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Jiang et al. (2022) studied Myocardial infarction (hypoxia-induced cardiomyocyte injury). miR-490-3p overexpression vs. Hypoxia treatment alone / control was evaluated on Cell viability, apoptosis, inflammatory responses, and injury markers. Overexpression of miR-490-3p alleviated hypoxia-induced cardiomyocyte injury, apoptosis, and inflammatory responses by directly targeting and downregulating FOXO1.
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