Endothelin-1 as Putative Modulator of Erectile Dysfunction. II. Calcium Mobilization in Cultured Human Corporal Smooth Muscle Cells

1995 ◽  
pp. 1571-1579 ◽  
Author(s):  
Weixin Zhao ◽  
George J. Christ
Keyword(s):  
Smooth Muscle ◽  
Erectile Dysfunction ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Calcium Mobilization ◽  
Endothelin 1

Effects of Histamine and Endothelin-1 on Membrane Potentials and Ion Currents in Bovine Tracheal Smooth-Muscle Cells

1998 ◽  
Vol 19 (5) ◽  
pp. 805-811 ◽  
Author(s):  
Masayuki Nara ◽  
Tsukasa Sasaki ◽  
Sanae Shimura ◽  
Takako Oshiro ◽  
Toshiya Irokawa ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Membrane Potentials ◽  
Tracheal Smooth Muscle ◽  
Ion Currents ◽  
Endothelin 1

Actin reorganization in airway smooth muscle cells involves Gq and Gi-2 activation of Rho

1999 ◽  
Vol 277 (3) ◽  
pp. L653-L661 ◽  
Author(s):  
Carol A. Hirshman ◽  
Charles W. Emala
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Actin Polymerization ◽  
Muscle Cells ◽  
Fiber Formation ◽  
Airway Smooth Muscle Cells ◽  
Actin Reorganization ◽  
Endothelin 1 ◽  
In Cells

Extracellular stimuli induce cytoskeleton reorganization (stress-fiber formation) in cells and Ca2+ sensitization in intact smooth muscle preparations by activating signaling pathways that involve Rho proteins, a subfamily of the Ras superfamily of monomeric G proteins. In airway smooth muscle, the agonists responsible for cytoskeletal reorganization via actin polymerization are poorly understood. Carbachol-, lysophosphatidic acid (LPA)-, and endothelin-1-induced increases in filamentous actin staining are indicative of actin reorganization (filamentous-to-globular actin ratios of 2.4 ± 0.3 in control cells, 6.7 ± 0.8 with carbachol, 7.2 ± 0.8 with LPA, and 7.4 ± 0.9 with endothelin-1; P < 0.001; n = 14 experiments). Although the effect of all agonists was blocked by C3 exoenzyme (inactivator of Rho), only carbachol was blocked by pertussis toxin. Although carbachol-induced actin reorganization was blocked in cells pretreated with antisense oligonucleotides directed against Gαi-2 alone, LPA- and endothelin-1-induced actin reorganization were only blocked when both Gαi-2 and Gqα were depleted. These data indicate that in human airway smooth muscle cells, carbachol induces actin reorganization via a Gαi-2pathway, whereas LPA or endothelin-1 induce actin reorganization via either a Gαi-2 or a Gqα pathway.

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