Key result
miR-26b overexpression reduces post-MI fibrosis in rats by targeting HMGA2 and suppressing fibroblast activation.
Why the study?
The role of miR-26b in myocardial infarction-induced myocardial fibrosis and its underlying molecular mechanisms were unknown.
p-value: p=<0.01
miR-26b overexpression ameliorates myocardial infarction-induced fibrosis by targeting HMGA2 and suppressing cardiac fibroblast activation in a rat model.
miR-26b may attenuate post-MI fibrosis in rats; hypothesis-generating and leaves open any clinical role pending human data.
BACKGROUND: Myocardial Fibrosis (MF) is an important physiological change after myocardial infarction (MI). MicroRNA-26b (MiR-26b) has a certain inhibitory effect on pulmonary fibrosis. However, the role of miR-26b in MI-induced MF rats and underlying molecular mechanisms remain unknown. METHODS: Forty male Sprague Dawley (SD) rats weighing 200-250 g were divided into four groups (n=10): Sham group, MF group, MF + negative control (NC) agomir group and MF + miR-26b agomir group. Cardiac fibroblasts were isolated from cardiac tissue. Fibrosis levels were detected by MASSON staining, while the expression of related genes was detected by RT-qPCR, Western blotting and Immunohistochemistry, respectively. TargetScan and dual-luciferase reporter assay were utilized to predict the relationship between miR-26b and high mobility group, AT-hook 2 (HMGA2). RESULTS: The study found the expression of miR-26b to be down-regulated in the myocardium of MF rats (P<0.01). miR-26b overexpression in vitro significantly reduced the survival rate of cardiac fibroblasts and inhibited the expression of the fibrillar-associated protein (α-SMA alphasmooth muscle actin (α-SMA) and collagen I) (P<0.01). TargetScan indicated that HMGA2 was one of the target genes of miR-26b; dual-luciferase reporter assay further confirmed the targeted regulatory relationship (P<0.01). Moreover, miR-26b overexpression significantly reduced the expression of HMGA2 (P<0.01). Notably, HMGA2 overexpression reversed the inhibitory effect of miR-26b overexpression on cardiac fibroblast viability and the expression of α-SMA and collagen I (P<0.01). Animal experiments further indicated that miR-26b overexpression inhibited MIinduced rat MF by inhibiting the expression of HMGA2 (P<0.05, P<0.01). CONCLUSION: In short, these findings indicate that miR-26b targets HMGA2 to ameliorate MI-induced fibrosis by suppression of cardiac fibroblasts activation.
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Ding et al. (2020) studied Myocardial Infarction-induced Fibrosis (n=40). miR-26b agomir vs. Sham, MF, and MF + negative control agomir was evaluated on Myocardial fibrosis and cardiac fibroblast activation (p=<0.01). Overexpression of miR-26b ameliorated myocardial infarction-induced fibrosis in rats by targeting HMGA2 and suppressing cardiac fibroblast activation (P<0.01).
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