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TRPC5 Does Not Cause or Aggravate Glomerular Disease.


ABSTRACT: Transient receptor potential channel 5 (TRPC5) is highly expressed in brain and kidney and mediates calcium influx and promotes cell migration. In the kidney, loss of TRPC5 function has been reported to benefit kidney filter dynamics by balancing podocyte cytoskeletal remodeling. However, in vivo gain-in-function studies of TRPC5 with respect to kidney function have not been reported. To address this gap, we developed two transgenic mouse models on the C57BL/6 background by overexpressing either wild-type TRPC5 or a TRPC5 ion-pore mutant. Compared with nontransgenic controls, neither transgenic model exhibited an increase in proteinuria at 8 months of age or a difference in LPS-induced albuminuria. Moreover, activation of TRPC5 by Englerin A did not stimulate proteinuria, and inhibition of TRPC5 by ML204 did not significantly lower the level of LPS-induced proteinuria in any group. Collectively, these data suggest that the overexpression or activation of the TRPC5 ion channel does not cause kidney barrier injury or aggravate such injury under pathologic conditions.

SUBMITTER: Wang X 

PROVIDER: S-EPMC5791075 | biostudies-literature | 2018 Feb

REPOSITORIES: biostudies-literature

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TRPC5 Does Not Cause or Aggravate Glomerular Disease.

Wang Xuexiang X   Dande Ranadheer R RR   Yu Hao H   Samelko Beata B   Miller Rachel E RE   Altintas Mehmet M MM   Reiser Jochen J  

Journal of the American Society of Nephrology : JASN 20171023 2


Transient receptor potential channel 5 (TRPC5) is highly expressed in brain and kidney and mediates calcium influx and promotes cell migration. In the kidney, loss of TRPC5 function has been reported to benefit kidney filter dynamics by balancing podocyte cytoskeletal remodeling. However, <i>in vivo</i> gain-in-function studies of TRPC5 with respect to kidney function have not been reported. To address this gap, we developed two transgenic mouse models on the C57BL/6 background by overexpressing  ...[more]

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