Mechanism of podocyte injury induced by Ephrin-B1 stimulation (IMAGE)
Caption
Stimulation of Ephrin-B1 induces the phosphorylation of Ephrin-B1 and nephrin independently of TRPC6-mediated Ca²⁺ influx. Phosphorylated Ephrin-B1 dissociates from nephrin and Par6. The released Par6 subsequently interacts with Cdc42, thereby enhancing Cdc42 activity. Increased Cdc42 activity promotes calcineurin (CaN) activity, which regulates the transcription factor Snail and reduces the mRNA expression of nephrin and Ephrin-B1. Increased Cdc42 activity also activates the transcription factor Stat3, leading to the induction of claudin-1 expression. A Cdc42 inhibitor prevents both the downregulation of nephrin and Ephrin-B1 expression and the induction of claudin-1 expression. In contrast, a CaN inhibitor and an angiotensin II type 1 receptor blocker (ARB) prevent the downregulation of nephrin and Ephrin-B1 expression but fail to prevent claudin-1 induction.
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Niigata University
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