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p38 MAPK pathway is involved in high glucose-induced thioredoxin interacting protein induction in mouse mesangial cells |
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| Authors: | Yunzhuo Ren Yuehua Wang Shuhui Wu Yanling Zhang |
| Institution: | a Department of Pathology, Hebei Medical University, No. 361 East Zhongshan Road, Shijiazhuang 050017, China b Department of Non-major Courses, Hebei Medical University, No. 361 East Zhongshan Road, Shijiazhuang 050017, China c Department of Nephrology, Third Hospital, Hebei Medical University, Shijiazhuang 050051, China |
| Abstract: | Excessive reactive oxygen species (ROS) play a key role in the pathogenesis of diabetic nephropathy. The thioredoxin (TRX) system, a major thiol antioxidant system, regulates the reduction of intracellular ROS. Here we show that high glucose (HG) inhibits TRX ROS-scavenging function through p38 mitogen-activated protein kinase (MAPK)-mediated induction of thioredoxin interacting protein (TXNIP) in mouse mesangial cells (MMCs). Knockdown of TXNIP in MMCs reversed HG-induced reduction of TRX activity and inhibited HG-induced activation of p38 MAPK and increased synthesis of TGF-β1 and fibronectin. These data suggest that HG-induced overexpression of TXNIP in MMCs, which may be via the p38 MAPK pathway. |
| Keywords: | TXNIP thioredoxin interacting protein TRX Thioredoxin HG high glucose MMC mouse mesangial cell DN diabetic nephropathy MAPK mitogen-activated protein kinase ROS reactive oxygen species |
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