Key result
Upregulation of miR-16 protected LPS-damaged H9c2 cells by increasing proliferation, reducing apoptosis, and decreasing inflammatory factors via CD40 and the NF-κB pathway.
Why the study?
The biological effect of miR-16 on myocarditis and its underlying molecular mechanism remained to be investigated.
Does upregulation of miR-16 protect against LPS-induced myocarditis injury in H9c2 cells?
Does upregulation of miR-16 protect against LPS-induced myocarditis injury in H9c2 cells?
Upregulation of miR-16 exerts protective anti-inflammatory and anti-apoptotic effects in an in vitro model of LPS-induced myocarditis via the CD40/NF-κB pathway.
miR-16 modulation may target inflammatory cardiomyocyte injury; leaves open clinical translation pending in vivo and human validation.
The purpose of this study was to investigate the biological effect of miR-16 on myocarditis and the underlying molecular mechanism. H9c2 cells were treated with 10 µg/mL lipopolysaccharide (LPS) for 12 hours to form a myocarditis injury model. We observed that LPS treatment distinctly decreased the level of miR-16 in H9c2 cells. Upregulation of miR-16 increased cell proliferation and reduced cell apoptosis. Then, CD40 was predicted and verified as a target gene of miR-16 by TargetScan and luciferase reporter assay, respectively. Furthermore, the messenger RNA and protein expression of CD40 are negatively regulated by miR-16. The relative expression of inflammatory factors was dramatically decreased by the miR-16 mimic. Cells cotransfected with miR-16 mimic and si-CD40 could significantly abolish the injury of cardiomyocytes caused by myocarditis. Our study illustrated that the upregulation of miR-16 has a protective effect on LPS-damaged H9c2 cells, which may be achieved by regulating CD40 and the nuclear factor kappa B pathway.
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Li et al. (2019) studied LPS-induced myocarditis. miR-16 mimic was evaluated on Cell proliferation, apoptosis, and inflammatory factor expression. Upregulation of miR-16 protected LPS-damaged H9c2 cells by increasing proliferation, reducing apoptosis, and decreasing inflammatory factors via CD40 and the NF-κB pathway.
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