scholarly journals Overexpression of transient receptor potential canonical type 1 (TRPC1) alters both store operated calcium entry and depolarization-evoked calcium signals in C2C12 cells

Cell Calcium ◽  
2011 ◽  
Vol 49 (6) ◽  
pp. 415-425 ◽  
Author(s):  
Tamás Oláh ◽  
János Fodor ◽  
Olga Ruzsnavszky ◽  
János Vincze ◽  
Celine Berbey ◽  
...  
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Calcium Entry ◽  
C2c12 Cells ◽  
Calcium Signals ◽  
Transient Receptor Potential Canonical ◽  
Store Operated Calcium Entry ◽  
Transient Receptor ◽  
Canonical Type

scholarly journals Up-Regulation of Transient Receptor Potential Canonical 1 (TRPC1) following Sarco(endo)plasmic Reticulum Ca2+ ATPase 2 Gene Silencing Promotes Cell Survival: A Potential Role for TRPC1 in Darier's Disease

2006 ◽  
Vol 17 (10) ◽  
pp. 4446-4458 ◽  
Author(s):  
Biswaranjan Pani ◽  
Eric Cornatzer ◽  
William Cornatzer ◽  
Dong-Min Shin ◽  
Mark R. Pittelkow ◽  
...  
Keyword(s):  
Cell Survival ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Calcium Entry ◽  
Hacat Cells ◽  
Transient Receptor Potential Canonical ◽  
Darier's Disease ◽  
Plasmic Reticulum ◽  
Store Operated Calcium Entry ◽  
Transient Receptor

The mechanism(s) involved in regulation of store operated calcium entry in Darier's disease (DD) is not known. We investigated the distribution and function of transient receptor potential canonical (TRPC) in epidermal skin cells. DD patients demonstrated up-regulation of TRPC1, but not TRPC3, in the squamous layers. Ca2+ influx was significantly higher in keratinocytes obtained from DD patients and showed enhanced proliferation compared with normal keratinocytes. Similar up-regulation of TRPC1 was also detected in epidermal layers of SERCA2+/− mice. HaCaT cells expressed TRPC1 in the plasma membrane. Expression of sarco(endo)plasmic reticulum Ca2+ ATPase (SERCA)2 small interfering RNA (siRNA) in HaCaT cells increased TRPC1 levels and thapsigargin-stimulated Ca2+ influx, which was blocked by store-operated calcium entry inhibitors. Thapsigargin-stimulated intracellular Ca2+ release was decreased in DD cells. DD keratinocytes exhibited increased cell survival upon thapsigargin treatment. Alternatively, overexpression of TRPC1 or SERCA2-siRNA in HaCaT cells demonstrated resistance to thapsigargin-induced apoptosis. These effects were dependent on external Ca2+ and activation of nuclear factor-κB. Isotretinoin reduced Ca2+ entry in HaCaT cells and decreased survival of HaCaT and DD keratinocytes. These findings put forward a novel consequence of compromised SERCA2 function in DD wherein up-regulation of TRPC1 augments cell proliferation and restrict apoptosis. We suggest that the anti-apoptotic effect of TRPC1 could potentially contribute to abnormal keratosis in DD.

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