Effects of BMP-7 on Id2 and E2A expression in NRK-52E cells exposed to high glucose
10.3969/j.issn.1000-4718.2016.02.022
- VernacularTitle:BMP-7对高糖环境下肾小管上皮细胞Id2和E2A蛋白表达的影响
- Author:
Lingping ZENG
;
Ying XIAO
;
Yingying ZHANG
;
Changzhi ZHANG
;
Depei WU
;
Yuanyuan LI
;
Mingjun SHI
;
Bing GUO
- Publication Type:Journal Article
- Keywords:
NRK-52E cells;
High glucose;
Bone morphogenetic protein-7;
Inhibitor of differentiation 2;
E2A
- From:
Chinese Journal of Pathophysiology
2016;32(2):321-326
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To investigate the effects of bone morphogenetic protein 7 ( BMP-7 ) on the expression of transcription factor E2A and inhibitor of differentiation 2 (Id2) in the renal tubule epithelial cells(NRK-52E)exposed to high glucose, and to explore its possible mechanism of improving renal tubular fibrosis induced by high glucose.METH-ODS:The NRK-52E cells were divided into control group, high glucose (HG) group and high glucose with different doses of BMP-7 (10μg/L and 20μg/L) group.The cells in HG group and BMP-7 group were cultured for 12 h, 24 h and 48 h. The protein expression of Id2, E2A, E-cadherin,α-smooth muscle actin (α-SMA) and collagen-I was detected by Western blot.In addition, the mRNA expression of Id2 was detected by real-time PCR.RESULTS:Compared with control group, the mRNA and protein levels of Id2 and the protein level of E-cadherin were down-regulated, while the protein levels of E2A,α-SMA and collagen-I were up-regulated in HG group (P<0.05).Compared with HG group, the mRNA and pro-tein levels of Id2 and the protein level of E-cadherin were significantly up-regulated, while the protein expression of E2A,α-SMA and collagen-I was significantly down-regulated in 20 μg/L BMP-7 group ( P<0.05 ) .The correlation analysis showed that the Id2 protein level was negatively correlated with the E2A protein level (P<0.05).CONCLUSION:BMP-7 may intercept the process of renal tubule fibrosis induced by high glucose via promoting the expression of Id2 and inhibi-ting the expression of E2A at protein level.