Fast calcium entry activation in denervated smooth muscle of the cat nictitating membrane

1989 ◽  
Vol 107 (5) ◽  
pp. 665-667
Author(s):  
A. K. Sibaev ◽  
R. Kh. Akhmedzyanov ◽  
Kh. S. Khamitov
Keyword(s):  
Smooth Muscle ◽  
Calcium Entry ◽  
Nictitating Membrane ◽  
Cat Nictitating Membrane

Regulation of postsynaptic alpha-1 adrenoceptors in smooth muscle of the cat nictitating membrane

1990 ◽  
Vol 21 (6) ◽  
pp. 514-518
Author(s):  
�. N. Telina ◽  
S. V. Kirshin ◽  
R. S. Nizamov ◽  
R. Kh. Akhmedzyanov ◽  
Kh. S. Khamitov
Keyword(s):  
Smooth Muscle ◽  
Nictitating Membrane ◽  
Cat Nictitating Membrane

Human esophageal smooth muscle shows capacitative calcium entry: Possffile involvement of TRP channels

2000 ◽  
Vol 118 (4) ◽  
pp. A858
Author(s):  
Jian Wang ◽  
Lisanne G. Laurier ◽  
Yang Jiao ◽  
Stephen M. Sims ◽  
Harold G. Preiksaitis
Keyword(s):  
Smooth Muscle ◽  
Trp Channels ◽  
Calcium Entry ◽  
Capacitative Calcium Entry

scholarly journals S1P activates store-operated calcium entry via receptor- and non-receptor-mediated pathways in vascular smooth muscle cells

2011 ◽  
Vol 300 (4) ◽  
pp. C919-C926 ◽  
Author(s):  
Kristen Park Hopson ◽  
Jessica Truelove ◽  
Jerold Chun ◽  
Yumei Wang ◽  
Christian Waeber
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Fluorescent Protein ◽  
Yellow Fluorescent Protein ◽  
Muscle Cells ◽  
Calcium Entry ◽  
Fluorescence Signal ◽  
Store Operated Calcium Entry

Sphingosine-1-phosphate (S1P) has been shown to modulate intracellular Ca2+ through both G protein-coupled receptors and intracellular second messenger pathways. The precise mechanism by which S1P activates store-operated calcium entry (SOCE) in vascular smooth muscle cells (VSMCs) has not been fully characterized. Because sphingolipids and Ca2+ modulate proliferation and constriction in VSMCs, characterizing the connection between S1P and SOCE may provide novel therapeutic targets for vascular diseases. We found that S1P triggered STIM1 puncta formation and SOCE in VSMCs. S1P-activated SOCE was inhibited by 2-aminoethoxydiphenyl borate (2-APB), diethylstilbestrol (DES), and gadolinium (Gd3+). SOCE was observed in VSMCs lacking either S1P2 or S1P3 receptors, suggesting that S1P acts via multiple signaling pathways. Indeed, both extracellular and intracellular S1P application increased the total internal reflection fluorescence signal in VSMCs cells transfected with STIM1-yellow fluorescent protein in a 2-APB-sensitive manner. These data, and the fact that 2-APB, DES, and Gd3+ all inhibited S1P-induced cerebral artery constriction, suggest that SOCE modulates S1P-induced vasoconstriction in vivo. Finally, S1P-induced SOCE was larger in proliferative than in contractile VSMCs, correlating with increases in STIM1, Orai1, S1P1, and S1P3 receptor mRNA. These data demonstrate that S1P can act through both receptors and a novel intracellular pathway to activate SOCE. Because S1P-induced SOCE contributes to vessel constriction and is increased in proliferative VSMCs, it is likely that S1P/SOCE signaling in proliferative VSMCs may play a role in vascular dysfunction such as atherosclerosis and diabetes.

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