Key result
Overexpression of miR-499-5p significantly inhibited hypoxia/reoxygenation-induced apoptosis and reduced injury markers in H9c2 cardiomyocytes by targeting SOX6.
Why the study?
Although miR-499 is known to be expressed in cardiomyocytes and increase after acute myocardial infarction, its role in hypoxia/reoxygenation-induced cardiomyocyte injury remained unclear.
Does miR-499-5p overexpression reduce hypoxia/reoxygenation-induced injury and apoptosis in rat H9c2 cardiomyocytes?
Does miR-499-5p overexpression reduce hypoxia/reoxygenation-induced injury and apoptosis in rat H9c2 cardiomyocytes?
p-value: p=<0.01
miR-499-5p protects cardiomyocytes from hypoxia/reoxygenation injury by downregulating SOX6, highlighting a potential therapeutic target for acute myocardial infarction.
Hypothesis-generating for miR-499-5p cardioprotection; in vivo studies required before clinical translation.
OBJECTIVE: MiR-499 has been reported to be expressed only in cardiomyocytes, and its expression would increase after acute myocardial infarction (AMI). miR-499 plays a role in the process of cardiomyocytes injury induced by hypoxia/reoxygenation (H/R), however, it still remains unclear. RESULTS: Hypoxia inhibited miR-499-5p expression and H/R induced apoptosis. SOX6 was a target gene of miR-499-5p, and high expression of miR-499-5p inhibited the expression of SOX6. MiR-499-5p reduced H9c2 cells injury by inhibiting the expression of SOX6, overexpression of which could reverse the effect of miR-499-5p on H9c2 cells. MiR-499-5p inhibited the levels of LDH and MDA, while overexpression of miR-499-5p inhibited H/R-induced cell apoptosis. MiR-499-5p could up-regulate the level of Bcl-2 and down-regulate the expression levels of Bax and caspase-3. However, SOX6 partially reversed these effects of miR-499-5p. CONCLUSION: We proved that miR-499-5p inhibited H/R-induced cardiomyocytes injury by targeting SOX6. Our results suggested that miR-499-5p/SOX6 pathway may present a potential therapeutic target for the treatment of AMI.
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Shi et al. (2019) studied Hypoxia/reoxygenation induced cardiomyocytes injury. miR-499-5p mimic vs. Mock sequence / Control was evaluated on Cell apoptosis and injury markers (LDH, MDA) (p=<0.01). Overexpression of miR-499-5p significantly inhibited hypoxia/reoxygenation-induced apoptosis and reduced injury markers in H9c2 cardiomyocytes by targeting SOX6.
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