miR ‐203 accelerates apoptosis and inflammation induced by LPS via targeting NFIL3 in cardiomyocytes

1. LPS induced the expression of miR ‐203 in H9c2 cells. 2. MiR‐203 promoted apoptosis and inflammatory responses induced by LPS. 3. Knockdown of nuclear factor interleukin‐3 (NFIL3) partly abrogated cardiac protective function of miR‐203. AbstractMyocarditis is an inflammatory disease of the myocardium. MicroRNA ‐203 (miR‐203) is involved in various physiological and pathological processes. In this work, we aimed to explore the roles and potential mechanisms of miR‐203 in myocarditis in vitro. Cardiomyocyte H9c2 was subjected to 10 μg/mL lipopolysaccharide (LPS) for 24 hours. Real‐time polymera se chain reaction analysis revealed that LPS upregulated miR‐203 expression in H9c2 cells. Cell counting kit‐8 (CCK‐8) and lactate dehydrogenase (LDH) assays demonstrated that inhibition of miR‐203 reduced cell injury induced by LPS. The cell apoptosis rate, caspase 3 activity, caspase 3/7 a ctivities, and the expression of cleaved‐caspase 3 (c‐caspase 3) were declined upon miR‐203 depletion. In addition, miR‐203 silencing attenuated the expression and production of inflammatory cytokines (tumor necrosis factor‐α, interleukin [IL]‐6, and IL‐8). On the contrary, overexpre ssion of miR‐203 showed the opposite trend in cell apoptosis and inflammation. Luciferase reporter assay confirmed that miR‐203 could bind with the nuclear factor interleukin‐3 (NFIL3) 3′‐untranslated regions (3′‐UTR), and miR‐203 regulated the expression of...
Source: Journal of Cellular Biochemistry - Category: Biochemistry Authors: Tags: RESEARCH ARTICLE Source Type: research