Role of gap junction protein connexin43 in podocyte injury

2016 Fiscal Year Final Research Report

• Project/Area Number: 26461219
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Kidney internal medicine
• Research Institution: University of Yamanashi
• Principal Investigator: YAO Jian 山梨大学, 総合研究部, 准教授 (50303128)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 腎臓 / 足細胞 / ギャップ結合 / 細胞傷害 / 酸化ストレス / TXNIP / P38 / ヘミチャネル

Outline of Final Research Achievements

Podocyte injury have been implicated in many types of human and experimental glomerulonephritis. Currently, the molecular mechanisms involved are still incompletely understood. In this study, we investigated the potential roles and mechanisms of gap junction protein connexin43 in podocyte injury. We found that induction of podocyte injury was associated with a marked increased expression of connexin43 that could be prevented by antioxidants. Conversely, inhibition or downregulation of Cx43 improved cellular oxidative status and attenuated oxidative injury. This effect of Cx43 could be related to the altered expression of TXNIP, a negative regulator of thioredoxin, and hemichannel-mediated extracellular release of GSH. Our study thus characterizes Cx43 as an important molecule involved in the regulation of oxidative podocyte injury.

Free Research Field

医歯薬学