miR-455 Promotes Cardiac Hypertrophy Induced by Short-term Overloaded Pressure in Experimental Mice
10.3969/j.issn.1000-3614.2015.09.016
- VernacularTitle:探讨微小核糖核酸-455在压力超负荷诱导的心肌肥厚小鼠模型中的作用机制
- Author:
Chuntao WU
;
Yongjun LI
;
Su LIU
;
Zhiyong WANG
- Publication Type:Journal Article
- Keywords:
microRNA;
Cardiac hypertrophy;
Calreticulin
- From:
Chinese Circulation Journal
2015;(9):889-894
- CountryChina
- Language:Chinese
-
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 groups:①TAC + 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,P<0.01, increased left ventricular diastolic (LVD) wall thicknesses (1.782 ± 0.058) mm vs (1.457 ± 0.050) mm,P<0.05, decreased LVD diameter (3.027 ± 0.052) mm vs (3.142±0.050) mm,P<0.05, increased LVEF (84.167 ± 4.167) % vs (77.000 ± 3.347) %,P<0.05; increased gene expressions of cardiac hypertrophy and ifbrosis, allP<0.05, decreased anti-apoptosis protein and increased promoting apoptosis protein, allP<0.05. Compared with TAC+GFP group, TAC+miR-455 group presented increased ratio of heart weight/body weight (12.04 ± 0.11) mg/g vs (9.78 ± 0.20) mg/g,P<0.01, increased LVD wall thicknesses (1.908 ± 0.062) mm vs (1.782 ± 0.058) mm,P<0.01, decreased LVD diameter (2.893 ± 0.069) mm vs (3.027 ± 0.052) mm,P<0.01, while LVEF was similar between 2 groups,P>0.05; increased gene expression of cardiac hypertrophy,P<0.05, while gene expression of cardiac ifbrosis was similar between 2 groups,P>0.05; 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), allP<0.01. Compared with TAC+GFP group, TAC+miR-455 group had decreased mRNA and protein expressions of CALR, bothP<0.01, while GRP78 protein expression was similar between 2 groups,P>0.05. Conclusion: miR-455 may promote cardiac hypertrophy induced by short-term overload pressure via targeting CALR in experimental mice.
