Activation of TGR5 reduces high glucose-induced cardiomyocyte hyper-trophy by inhibiting CaN/NFAT3 signaling
10.3969/j.issn.1000-4718.2017.02.008
- VernacularTitle:激活 TGR5通过 CaN／NFAT3途径减轻高糖诱导的心肌细胞肥大
- Author:
Jian FENG
;
Dan WU
;
Xuxin CHEN
;
Yi ZHONG
;
Yingcai LIU
;
Jiafu LI
- Keywords:
G-protein-coupled receptors;
TGR5;
Cardiomyocyte hypertrophy;
High glucose;
Calcineurin;
Nuclear factor of activated T-cells 3
- From:
Chinese Journal of Pathophysiology
2017;33(2):239-243
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To investigate the role of G-protein-coupled bile acid receptor 1 ( GPBR1; also known as TGR5) activation in high glucose-induced cardiomyocyte hypertrophy and calcineurin (CaN)/nuclear factor of activated T-cells 3 (NFAT3) signaling.METHODS:Primarily cultured mouse cardiomyocytes were used in the study .The cell surface areas of the cardiomyocytes were measured by an image analysis system .The cell protein content was detected by BCA meth-od.The expression of TGR5, CaN and NFAT3 at mRNA and protein levels was determined by RT-PCR and Western blot . RESULTS:The mouse cardiomyocytes were successfully cultured .High glucose significantly induced the increases in the cell surface area, the cell protein content and the expression of CaN and NFAT 3 (P<0.05) in the cardiomyocytes.TGR5 activation or a CaN antagonist cyclosporin A inhibited high glucose-induced cardiomyocyte hypertrophy and the expression of CaN and NFAT3 (P<0.05).These effects of TGR5 activation were abolished by TGR5 gene interference (P<0.05). CONCLUSION:TGR5 activation reduces high glucose-induced cardiomyocyte hypertrophy by inhibiting CaN /NFAT3 sig-naling.
