| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| 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.
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