Effect and Mechanism of Rapamycin Inhibiting mTOR on Heart Valve Cell Calcification in Experimental Rats
10.3969/j.issn.1000-3614.2015.09.018
- VernacularTitle:探讨雷帕霉素靶向抑制mTOR对大鼠心瓣膜细胞钙化的影响及其作用机制
- Author:
Yan TAN
;
Jiye WANG
;
Renliang YI
;
Jian QIU
- Publication Type:Journal Article
- Keywords:
Mammalian target of RAPA;
Rapamycin;
Heart valve cell;
Cell calciifcation
- From:
Chinese Circulation Journal
2015;(9):900-903
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effect and mechanism of rapamycin inhibiting mammalian target of RAPA (mTOR) on heart valve cell calciifcation in experimental rats. Methods: The rat’s valvular interstitial cells were isolated and the cells were cultured in 4 groups:①Normal control group,②Calciifcation group,③Rapamycin group and ④Calciifcation + rapamycin group. The apoptosis rates of valvular interstitial cells were detected by flow cytometry, calcium deposition was observed by Alizarin S staining, the calcified nodules were counted and the protein expressions of bmp-2, osteocalcin, osteopontin, smad-1 and caspase-3 were examined by Western blot analysis. Results: The rat's valvular interstitial cells were suceessfully isolated; the cell apoptosis rates were similar among different groups,P>0.05. The calciifed nodule in Calciifcation group (0.471 ± 0.091) was more than Normal control group (0.104 ± 0.023), while the nodule in Calciifcation + rapamycin group (0.237 ± 0.039) was less than Calciifcation group, allP<0.05. Compared with Normal control group, the protein expression levels of bmp-2, osteopontin and smad-1 were obviously increased in Calciifcation group,P<0.05, and compared with Calciifcation group, the above indexes were obviously lower in Calciifcation + rapamycin group, P<0.05. The protein expression levels of caspase-3 were similar among 3 experimental groups,P>0.05. Conclusion: Rapamycin may down-regulate the targeting protein expressions of bmp-2, osteopontin and smad-1 via inhibiting mTOR, therefore, reducing the valvular interstitial cell calcification which might be related to mTOR pathway suppression in experimental rats.
