miR-455 Promotes Cardiac Hypertrophy Induced by Short-term Overloaded Pressure in Experimental Mice / 中国循环杂志

ABSTRACT

Objective: To investigate the role of miR-455 in cardiac hypertrophy with its potential cellular and molecular mechanism in mice. Methods: The mice model of cardiac hypertrophy was established by transverse aorta constriction (TAC), and 18 male kunming TAC mice were randomly divided into 3 groups①TAC + miR-455 group,②TAC + GFP (green lfuorescence protein) group and③Sham group (sham operation + GFP).n=6 in each group and all animals were treated for 2 weeks. The hemodynamic and echocardiographic indexes were examined, histo-pathological changes of myocardial tissue were observed by HE and Masson staining. The hypertrophic and ifbrosis gene expressions were measured by RT-PCR, the apoptosis protein level was detected by Western blot analysis. The expressions of miR-455 targeting gene and protein were also determined. Results: Upon 2 weeks modeling, compared with Sham group, TAC+GFP group had increased ratio of heart weight/ body weight (9.78 ± 0.20) mg/g vs (8.25 ± 0.22) mg/g,P0.05; increased gene expression of cardiac hypertrophy,P0.05; the anti-apoptosis protein and promoting apoptosis protein expressions were similar between 2 groups. Compared with Sham group, TAC+GFP group had increased expressions of calreticulin (CALR) and glucose-regulated protein 78 (GRP78), allP0.05. Conclusion: miR-455 may promote cardiac hypertrophy induced by short-term overload pressure via targeting CALR in experimental mice.