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Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Cell+Physiol 2015 ; 230 (6): 1389-99 Nephropedia Template TP
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Phospholipase C Epsilon (PLC?) Induced TRPC6 Activation: A Common but Redundant Mechanism in Primary Podocytes #MMPMID25521631
Kalwa H; Storch U; Demleitner J; Fiedler S; Mayer T; Kannler M; Fahlbusch M; Barth H; Smrcka A; Hildebrandt F; Gudermann T; Dietrich A
J Cell Physiol 2015[Jun]; 230 (6): 1389-99 PMID25521631show ga
In eukaryotic cells, activation of phospholipase C (PLC)-coupled membrane receptors by hormones leads to an increase in the intracellular Ca2+ concentration [Ca2+]i. Catalytic activity of PLCs results in the hydrolysis of phosphatidylinositol 4,5-bisphosphate to generate inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG) which opens DAG-sensitive classical transient receptor channels 3, 6, and 7 (TRPC3/6/7), initiating Ca2+ influx from the extracellular space. Patients with focal segmental glomerulosclerosis (FSGS) express gain-of-function mutants of TRPC6, while others carry loss-of-function mutants of PLC?, raising the intriguing possibility that both proteins interact and might work in the same signalling pathway. While TRPC6 activation by PLC? and PLC? isozymes was extensively studied, the role of PLC? in TRPC6 activation remains elusive. TRPC6 was co-immunoprecipitated with PLC? in a heterologous overexpression system in HEK293 cells as well as in freshly isolated murine podocytes. Receptor-operated TRPC6 currents in HEK293 cells expressing TRPC6 were reduced by a specific PLC? siRNA and by a PLC? loss-of-function mutant isolated from a patient with FSGS. PLC?-induced TRPC6 activation was also identified in murine embryonic fibroblasts (MEFs) lacking G?q/11 proteins. Further analysis of the signal transduction pathway revealed a G?12/13 Rho-GEF activation which induced Rho-mediated PLC? stimulation. Therefore, we identified a new pathway for TRPC6 activation by PLC?. PLC?-/- podocytes however, were undistinguishable from WT podocytes in their angiotensin II-induced formation of actin stress fibers and their GTP?S-induced TRPC6 activation, pointing to a redundant role of PLC?-mediated TRPC6 activation at least in podocytes.
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J+Cell+Physiol 2015 ; 230 (6): 1389-99
