RPC6 Up-Regulation in Ang II-Induced Podocyte Apoptosis Might Result from ERK Activation and NF-κB Translocation

• DOI: 10.3181/0901-rm-11
• Publication Date: 2009-06-23T01:55:52Z
• Authors: Han Zhang; Jie Ding; Qingfeng Fan; Shufang Liu
• Keywords: 0301 basic medicine; Pyrrolidines; Podocytes; Angiotensin II; NF-kappa B p50 Subunit; Apoptosis; Cell Line; Up-Regulation; Mice; 03 medical and health sciences; Thiocarbamates; Nitriles; Butadienes; TRPC6 Cation Channel; Animals; Calcium; Enzyme Inhibitors; Extracellular Signal-Regulated MAP Kinases; TRPC Cation Channels

Angiotensin II (Ang II) has been recognized as an apoptosis inducer in podocytes, but the mechanism of induced by Ang is unclear. Transient receptor potential cation channel 6 (TRPC6) a calcium located podocyte membrane. The present study evaluated alteration TRPC6 expression and Ca(2+) influx involved II-induced apoptosis. possible pathways related to were also investigated. mouse podocytes (MPC5) was II. protein level increased markedly response stimulation, intracellular concentration elevated. By transfection with siRNA, transient inhibited. Treated extracellular signal-regulated kinase (ERK) pathway specific inhibitor U0126 or nuclear factor-kappaB (NF-kappaB) ammonium pyrrolidinedithiocarbamate (PDTC) II, respectively not only up-regulation reduced, decreased. Moreover, translocation NF-kappaB nucleus resulted from reduced treatment U0126. In conclusion, enhancement well mediated channels contributed activation ERK subsequent possibly necessary for