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Role of TRPC6 in High Glucose‐Induced Podocyte Apoptosis
Author(s) -
Liu BingChen,
Song Xiang,
Yang LiLi,
Eaton Douglas,
Ma HePing
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1143.12
Subject(s) - trpc6 , podocyte , reactive oxygen species , apoptosis , chemistry , intracellular , microbiology and biotechnology , small hairpin rna , medicine , endocrinology , biology , biochemistry , receptor , kidney , transient receptor potential channel , gene knockdown , proteinuria
It has been reported that the number of podocytes is significantly reduced in diabetic patients and animal models. However, the mechanism remains unclear. In the present study, we found that high glucose induced apoptosis in control podocytes which express TRPC6 channels, but not in TRPC6 − podocytes in which TRPC6 was knocked down by its shRNA. This effect was reproduced by treatment of the podocytes with hydrogen peroxide (H 2 O 2 ), one form of reactive oxygen species (ROS). Single‐channel data from cell‐attached patch‐clamp experiments showed that high glucose activated the TRPC6 channel, which was mimicked by exposure of podocytes to H 2 O 2 . Confocal microscopy data showed that high glucose elevated ROS in podocytes and H 2 O 2 elevated intracellular Ca 2+ via activation of TRPC6. These data together suggest that high glucose induces apoptosis in podocytes by inducing TRPC6 activity and subsequently increasing intracellular Ca 2+ via elevation of ROS.