Effect of Fibroblast Growth Factor 21 on Endoplasmic Reticulum Stress Induced Rat's H9c2 Cardiomyocyte Apoptosis With its Mechanism
10.3969/j.issn.1000-3614.2017.03.017
- VernacularTitle:成纤维细胞生长因子21对内质网应激诱导心肌细胞凋亡的影响及其机制研究
- Author:
Pingping LIANG
;
Lin ZHONG
;
Lei GONG
;
Jiahui WANG
;
Jun YANG
- Keywords:
Fibroblast growth factor;
Endoplasmic reticulum;
Myocyte;
cardiac;
Apoptosis
- From:
Chinese Circulation Journal
2017;32(3):279-283
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To explore the protective roll of ifbroblast growth factor 21 (FGF21) in endoplasmic reticulum stress (ERS) induced rat's H9c2 cardiomyocyte apoptosis with its mechanism. Methods: pcDNA4 was used as gene vector, pcDNA4-FGF21 plasmid was constructed and transfected into rat's H9c2 myocardiocytes for 48 h. ERS model was established by 10 μM tunicamycin (TM) induction for 24 h. The experiment was conducted in 4 groups:①Control group,②TM group, the cells were treated by TM,③pcDNA4-FGF21+TM group,④pcDNA4+TM group. The expressions of FGF21, protein kinase R-like ER kinase (PERK) and c-Jun N-terminal kinases (JNK) mediated apoptosis pathway related protein were measured by Western blot analysis; cell survival rate was examined by CCK-8 method and apoptosis rate was detected by TUNEL technique. Results: pcDNA4-FGF21 vector was successfully constructed and overexpressed in H9c2 myocardiocytes. Compared with Control group, TM group and pcDNA4+TM group had up-regulated endogenous FGF21 expression, increased PERK and JNK mediated apoptosis pathway related protein expression; reduced cell survival rate and elevated apoptosis rate. Compared with TM group and pcDNA4+TM group, pcDNA4-FGF21+TM group had down-regulated PERK and JNK mediated apoptosis pathway related protein expression; increased cell survival rate and decreased apoptosis rate. Conclusion: FGF21 overexpression can reduce ERS induced apoptosis rat's H9c2 myocardiocytes which might be partly related for inhibiting PERK and JNK mediated signal transduction of apoptosis pathway.
