Mediation of inflammatory activation of renal tubular epithelial cells by high mobility group protein box 1 interacting with Toll-like receptor 4
10.3760/cma.j.issn.1001-7097.2015.11.005
- VernacularTitle:高迁移率族蛋白B1通过Toll样受体4介导肾小管上皮细胞的炎性反应
- Author:
Shixiang ZHENG
;
Qian YANG
;
Hongxia YANG
;
Qin ZHANG
;
Guohua DING
- Publication Type:Journal Article
- Keywords:
Inflammation;
Toll-like receptor 4;
HMGB1 protein;
Renal tubular epithelial cells
- From:
Chinese Journal of Nephrology
2015;31(11):828-834
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe functional changes of renal tubular epithelial cells stimulated by high mobility group protein box 1 (HMGB1) and associated mechanism.Methods Renal tubular epithelial cells (NRK52E) were divided into control group,HMGB1 group and HMGB1+ lipopolysaccharide from Rhodobactersphaeroides (LPS RS) group.Toll-like receptor 4 (TLR4) expression was detected by immunofluorescence and Western blotting.Apoptosis rate and cell cycle arrest were identified with flow cytometry.The activation of MAPK signaling pathway and NF-κB were detected by Western blotting.The IL-1,IL-6 and tissue inhibitor of metalloproteinases 2 (TIMP2) mRNA levels were measured by real-time PCR.The secretion levels of IL-1,IL-6 and TIMP2 were measured by protein chips assay.Results TLR4 was expressed by NRK52E cells.Compared with the control group,there were increased cell cycle G1 arrest,MAPK signaling pathway and NF-κB activation in HMGB1 group.Furthermore,IL-1,IL-6 and TIMP2 mRNA levels were increased and IL-1,IL-6 and TIMP2 were secreted by NRK52E when stimulated with HMGB1 (all P ＜0.05).However,effects mediated by HMGB1 stimulation could be inhibited by LPS RS (all P＜0.05).Conclusions Inflammatory activation of NRK52E cells can be mediated by the interaction of HMGB1 and TLR4.
