Uromodulin aggravates renal tubulointerstitial injury through activation of the complement pathway in rats

塔姆-霍斯法尔蛋白 补体系统 替代补体途径 免疫印迹 纤维化 医学 污渍 内科学 病理 内分泌学 化学 免疫学 生物化学 免疫系统 基因
作者
Yu Li,Fei Pei,Qiaoling Sun,Fei Shen,Xiangdong Yang,Zhao Hu,Maojing Liu
出处
期刊:Journal of Cellular Physiology [Wiley]
卷期号:236 (7): 5012-5021 被引量:4
标识
DOI:10.1002/jcp.30208
摘要

Uromodulin (Umod) is the most abundant constituent of urine in humans and exclusively found in the kidney tubular epithelium. However, the specific role of Umod in renal tubulointerstitial injury is yet to be understood. The present study was conducted with aim of investigating the potential therapeutic mechanism of Umod in the regulation of renal tubulointerstitial injury. Protein expression of Umod in renal tubular epithelial cells was measured with the conduction of Western blot analysis. Enzyme-linked immunosorbent assay and immunofluorescence assay were performed to detect the complement activation products and the activation products of surface deposition. The expression of C1q, C2, C4, B factor, C3, C5, H factor, CD46, CD55, C3aR, and C5aR were determined with the use of reverse-transcription quantitative polymerase chain reaction and Western blot analyses. Subsequently, the unilateral ureteral obstruction (UUO) rat model was established. Renal tubulointerstitial injury was assessed with the application of hematoxylin-eosin staining and Masson staining in rats. UUO rats and normal rats were injected with si-NC or si-Umod and complement inhibitor. UUO rats were observed to have serious impairment of kidney tubule, renal tubular dilation, and epithelial atrophy, with downregulated Umod and activated complement pathway. Silencing of Umod resulted in the activation of complement system while promoting interstitial fibrosis in renal tubules. Moreover, addition of complement inhibitor significantly alleviated the renal tubule injury and fibrosis. Collectively, our study suggests that silencing of Umod mediates the complement pathway, exacerbating renal tubulointerstitial injury in rats, which provides insight into the development of novel therapeutic agents for renal tubulointerstitial injury.
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