693: Increased expression of transient receptor vanilloid channels during pregnancy regulates uterine smooth muscle cell calcium entry and contraction

2009 ◽  
Vol 201 (6) ◽  
pp. S251
Author(s):  
Margaux Becard ◽  
Shu Chen Lyu ◽  
Cristina Alvira ◽  
Eloa Adams ◽  
Anita Umesh ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Calcium Entry ◽  
Uterine Smooth Muscle ◽  
Cell Calcium ◽  
Transient Receptor

scholarly journals Anthrax toxin receptor 2 promotes human uterine smooth muscle cell viability, migration and contractility

2014 ◽  
Vol 210 (2) ◽  
pp. 154.e1-154.e8 ◽  
Author(s):  
Joy Yumiko Vink ◽  
Pelisa Cheryll Charles-Horvath ◽  
Jan Krzysztof Kitajewski ◽  
Claire Vech Reeves
Keyword(s):  
Smooth Muscle ◽  
Cell Viability ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Anthrax Toxin ◽  
Uterine Smooth Muscle ◽  
Toxin Receptor ◽  
Anthrax Toxin Receptor 2

PDGF stimulates pulmonary vascular smooth muscle cell proliferation by upregulating TRPC6 expression

2003 ◽  
Vol 284 (2) ◽  
pp. C316-C330 ◽  
Author(s):  
Ying Yu ◽  
Michele Sweeney ◽  
Shen Zhang ◽  
Oleksandr Platoshyn ◽  
Judd Landsberg ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Transient Receptor Potential ◽  
Cyclopiazonic Acid ◽  
Receptor Potential ◽  
Protein Levels ◽  
Resultant Increase ◽  
Transient Receptor

Capacitative Ca2+ entry (CCE) through store-operated Ca2+ (SOC) channels plays an important role in returning Ca2+ to the sarcoplasmic reticulum (SR) and regulating cytosolic free Ca2+concentration ([Ca2+]cyt). A rise in [Ca2+]cyt and sufficient Ca2+ in the SR are required for pulmonary artery smooth muscle cell (PASMC) proliferation. We tested the hypothesis that platelet-derived growth factor (PDGF)-mediated PASMC growth involves upregulation of c-Jun and TRPC6, a transient receptor potential cation channel. In rat PASMC, PDGF (10 ng/ml for 0.5–48 h) phosphorylated signal transducer and activator of transcription (STAT3), increased mRNA and protein levels of c-Jun, and stimulated cell proliferation. PDGF treatment also upregulated TRPC6 expression and augmented CCE, elicited by passive depletion of Ca2+ from the SR using cyclopiazonic acid. Furthermore, overexpression of c-Jun stimulated TRPC6 expression and CCE amplitude in PASMC. Downregulation of TRPC6 using an antisense oligonucleotide specifically for human TRPC6 decreased CCE and inhibited PDGF-mediated PASMC proliferation. These results suggest that PDGF-mediated PASMC proliferation is associated with c-Jun/STAT3-induced upregulation of TRPC6 expression. The resultant increase in CCE raises [Ca2+]cyt, facilitates return of Ca2+ to the SR, and enhances PASMC growth.

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