Expression of WNT4 and its inhibitory factor SFRP1 in renal tissue of diabetic nephropathy rats
- VernacularTitle:WNT4及其抑制因子SFRP1在糖尿病肾病大鼠肾组织中的表达
- Author:
Jing KONG
1
;
Ping-Ping TIAN
;
Yuan-Yuan LI
;
Ming-Jun SHI
;
Yuan-Yuan WANG
;
Ying XIAO
;
Fan ZHANG
;
Bing GUO
;
Lan SUN
Author Information
1. 贵州医科大学 病理生理学教研室
- Keywords:
Diabetic nephropathy;
WNT4;
β-catenin;
SFRP1
- From:
Basic & Clinical Medicine
2018;38(2):194-199
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the change of expression of WNT4/β-catenin signaling pathway and its inhibitory factor secreted frizzled-related protein 1 (SFRP1) in renal tissue in diabetic nephropathy(DN) rats, and to explore its possible role in the development of renal fibrosis. Methods Rats were randomly divided into normal control(NC) group and DN group, and equipped with 8 in each group. The IDDM model was prepared by tail vein injection of STZ 55 mg/kg. Hemotoxyin and eosin、Periodic Acid-Schiff and Masson stain were used to observe the morphological structure and fibrotic lesions in renal tissue;Immunohistochemical analysis was used to observe the protein expression of WNT4 and β-catenin in renal tissue;Western blot was used to detect the protein expression changes of WNT4, SFRP1, β-catenin, p-GSK-3β, GSK-3β, Collagenl, a-SMA, E-cadherin in renal tissue in each group;The mRNA expression of WNT4 and SFRPl in renal tissues of rat was detected by realtime PCR. Results Compared with NC group, renal tissue fibrosis was obvious in DN group. Compared with NC group, the protein and mRNA expressions of WNT4 significantly increased (P＜0.05), the protein expressions of β-catenin, p-GSK-3β, α-SMA and collagen I significantly increased (P < 0.05), the protein expressions of Ecadherin significantly decreased (P＜0. 05), the protein and mRNA expression of SFRPl significantly decreased (P＜0.05). Conclusions In the case of DN, the signal pathway of WNT4/β-catenin is abnormal activation. The expression of SFRPl is decreased, and that may inhibit this pathway and promote the development of renal fibrosis in DN.
