Expression of response gene to complement 32 in renal tissue of children with IgA nephropathy and its significance
10.3760/cma.j.issn.1001-7097.2011.07.003
- VernacularTitle:RGC-32在儿童IgA肾病肾组织中的表达及意义
- Author:
Xiaoling NIU
;
Xinyu KUANG
;
Zhigang ZHANG
;
Xueguang LIU
;
Zhonghua ZHAO
;
Xin ZHANG
;
Hong XU
;
Wenyan HUANG
- Publication Type:Journal Article
- Keywords:
Glomerulonephritis,IgA;
Cell line,transformed;
Response gene complement 32;
Epithelial-mesenchymal transition
- From:
Chinese Journal of Nephrology
2011;27(7):479-483
- CountryChina
- Language:Chinese
-
Abstract:
Objective To examine the expression of response gene to complement 32 (RGC-32) in renal tissue of children with IgA nephropathy (IgAN), and to explore its significance. Methods The subjects were 45 children diagnosed as IgAN by renal biopsy. The expression of RGC-32, α-smooth muscle actin (α-SMA) and transforming growth factor β1 (TGF-β1) was examined by immunohistochemistry staining. The correlation of RGC-32 expression with α-SMA,TGF-β1, degree of renal pathological lesions and clinical index in IgAN was assessed by Spearman correlation analysis. Results RGC-32 protein located in renal tubular epithelial cells in normal and IgAN renal tissues. The positive expression index of RGC-32 in nomal group, IgAN mild group, moderate group and severe group was (18.29±6.22)%, (23.90±9.65)%, (31.23±9.86)%,and (34.52±10.63)% respectively. With more severity of renal pathological lesions, the expression of RGC-32 in IgAN was enhanced. The RGC-32 expression was positively correlated with the score of glomerulus and renal interstitium in children with IgAN (r=0.385, 0.347, P＜0.05), as well as α-SMA, TGF-β1 (r=0.594, 0.521, P＜0.01), but was not correlated with Scr, urinary NAG/Cr,Alb/Cr, IgG/Cr, and α1-M/Cr (r =0.117, -0.115, -0.138, -0.176, -0.028, all P ＞0.05).Conclusions RGC-32 protein locates in renal tubular epithelial cells in normal and IgAN renal tissues. RGC-32 may participate in the course of renal tubulointerstitial lesions in children with IgAN, especially in the course of epithelial-mesenchymal transition (EMT) induced by TGF-β1.
