Role of microRNA-215 in nephropathy of type 2 diabetic db/db mice
10.3760/cma.j.issn.1001-7097.2012.04.012
- VernacularTitle:microRNA-215在糖尿病肾病小鼠肾组织中的表达及意义
- Author:
Qi PANG
;
Jiao MU
;
Yanhong GUO
;
Jigang CHEN
;
Wei ZENG
;
Yongjun HUANG
;
Jun ZHANG
;
Dan QIAN
;
Bing FENG
- Publication Type:Journal Article
- Keywords:
Diabetic nephropathies;
MicroRNAs;
Beta catenin;
Interacting protein 1;
Luciferase reporter
- From:
Chinese Journal of Nephrology
2012;28(4):305-311
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the renal expression changes of microRNA-215(miR-215) and its role in diabetic nephmpathy of type 2 diabetic db/db mice. Methods Fourweek-old diabetic db/db mice and norml control group non-diabetic db/m mice were selected.Real-time PCR was used to detect the relative level of miR-215 at the age of 8,12 and 16 weeks.Catenin beta interacting protein 1 (CTNNBIP1) mRNA and protein level were measured by realtime PCR,WesteRN blotting and immunohistochemisty.A lueiferase reporter assay was used to determine whether CTNNBIP1 was a direct target of miR-215. Results (1)With the growth of db/db mice,the major pathological characteristics of kidney included glomerular hypertrophy,segmental mesangial cells proliferation and mesangial matrix expansion.(2)Compared with the db/m mice,the db/db mice of 8,12 and 16 weeks showed obvious increase in body weight(BW),blood glucose (Glu) and 24 hour urinary albumin excretion (UAE) (P＜0.05,respectively).(3)Compared with the db/m mice,special miR-215 was highly expressed in the kidney of db/db mice and was up-regulated significantly according to the development of DN (P＜0.05).(4)The mRNA and protein expression of CTNNBIPl of kidney were consistently down-regulated in db/db mice than those in controls (P＜0.05,respectively). (5)By luciferase reporter,miR-215 could negatively regulate CTNNBIP1 gene by targeting its 3'-UTR sequence (P＜0.01). Conclusion High expression level of miR-215 plays a potential role in the initiation and progression of DN by down-regulating the expression of CTNNBIPl.
