scholarly journals Physiological Induction of Transient Receptor Potential Canonical Proteins, Calcium Entry Channels, in Human Myometrium: Influence of Pregnancy, Labor, and Interleukin-1β

2004 ◽  
Vol 89 (3) ◽  
pp. 1291-1300 ◽  
Author(s):  
A. Dalrymple ◽  
D. M. Slater ◽  
L. Poston ◽  
R. M. Tribe
Keyword(s):  
Mrna Expression ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Calcium Entry ◽  
Human Myometrium ◽  
Physiological Regulation ◽  
Transient Receptor Potential Canonical ◽  
Active Labor ◽  
Transient Receptor ◽  
Trpc Proteins

Abstract This study investigated gestational regulation of transient receptor potential canonical (TrpC) proteins, putative calcium entry channels in human myometrium, and the potential modulation of TrpC expression by IL–1β, a cytokine implicated in labor. Total RNA and proteins were isolated from myometrial biopsies obtained from NP women, pregnant women at term not in labor (TNL), or term active labor (TAL) and from primary cultured human myometrial smooth muscle cells incubated with IL–1β or IL–1β with or without nimesulide. Semiquantitative RT-PCR demonstrated significant up-regulation of TrpC1 in TAL and TNL (P ≤ 0.01) and TrpC6 (P ≤ 0.01) and TrpC7 (P ≤ 0.05) in TAL samples. TrpC3 and TrpC4 mRNA expression was unaffected. Western blot demonstrated significant up-regulation of TrpC1 in TAL and TNL (P ≤ 0.05) and TrpC3 (P ≤ 0.01), TrpC4 (P ≤ 0.05), and TrpC6 (P ≤ 0.01) in TAL samples. IL–1β did not alter TrpC1, 3, 4, 6, or 7 mRNA expression; but IL–1β exclusively up-regulated TrpC3 protein expression (P ≤ 0.05). TrpC3 up-regulation was unaffected by cyclooxygenase blockade. These data demonstrate physiological regulation of TrpC mRNA and protein and suggest an important role for TrpC proteins in human myometrium during labor.

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.

scholarly journals Transient receptor potential canonical 5 (TRPC5) protects against pain and vascular inflammation in arthritis and joint inflammation

2016 ◽  
Vol 76 (1) ◽  
pp. 252-260 ◽  
Author(s):  
Khadija M Alawi ◽  
Fiona A Russell ◽  
Aisah A Aubdool ◽  
Salil Srivastava ◽  
Yanira Riffo-Vasquez ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Inflammatory Arthritis ◽  
Transient Receptor Potential ◽  
Vascular Inflammation ◽  
Receptor Potential ◽  
Joint Inflammation ◽  
Lavage Fluid ◽  
Transient Receptor Potential Canonical ◽  
Transient Receptor

ObjectiveTransient receptor potential canonical 5 (TRPC5) is functionally expressed on a range of cells including fibroblast-like synoviocytes, which play an important role in arthritis. A role for TRPC5 in inflammation has not been previously shown in vivo. We investigated the contribution of TRPC5 in arthritis.MethodsMale wild-type and TRPC5 knockout (KO) mice were used in a complete Freund's adjuvant (CFA)-induced unilateral arthritis model, assessed over 14 days. Arthritis was determined by measurement of knee joint diameter, hindlimb weightbearing asymmetry and pain behaviour. Separate studies involved chronic pharmacological antagonism of TRPC5 channels. Synovium from human postmortem control and inflammatory arthritis samples were investigated for TRPC5 gene expression.ResultsAt baseline, no differences were observed. CFA-induced arthritis resulted in increased synovitis in TRPC5 KO mice assessed by histology. Additionally, TRPC5 KO mice demonstrated reduced ispilateral weightbearing and nociceptive thresholds (thermal and mechanical) following CFA-induced arthritis. This was associated with increased mRNA expression of inflammatory mediators in the ipsilateral synovium and increased concentration of cytokines in synovial lavage fluid. Chronic treatment with ML204, a TRPC5 antagonist, augmented weightbearing asymmetry, secondary hyperalgesia and cytokine concentrations in the synovial lavage fluid. Synovia from human inflammatory arthritis demonstrated a reduction in TRPC5 mRNA expression.ConclusionsGenetic deletion or pharmacological blockade of TRPC5 results in an enhancement in joint inflammation and hyperalgesia. Our results suggest that activation of TRPC5 may be associated with an endogenous anti-inflammatory/analgesic pathway in inflammatory joint conditions.

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