Epithelial Modulation of Airway Smooth Muscle Response to Endothelin-1

1991 ◽  
Vol 144 (2) ◽  
pp. 373-378 ◽  
Author(s):  
Steven R. White ◽  
Darren P. Hathaway ◽  
Jason G. Umans ◽  
Julio Tallet ◽  
Cyril Abrahams ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Muscle Response ◽  
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.

scholarly journals Endothelin-1-induced potentiation of human airway smooth muscle proliferation: an ETA receptor-mediated phenomenon

1996 ◽  
Vol 118 (1) ◽  
pp. 191-197 ◽  
Author(s):  
Reynold A. Panettieri ◽  
Roy G. Goldie ◽  
Paul J. Rigby ◽  
Andrew J. Eszterhas ◽  
Douglas W.P. Hay
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Human Airway Smooth Muscle ◽  
Endothelin 1 ◽  
Human Airway ◽  
Smooth Muscle Proliferation ◽  
Eta Receptor

Contraction of human airway smooth muscle by endothelin-1 and IRL 1620: effect of bosentan

1997 ◽  
Vol 324 (2-3) ◽  
pp. 219-222 ◽  
Author(s):  
Tsuneyuki Takahashi ◽  
Peter J Barnes ◽  
Ivana Kawikova ◽  
Magdi H Yacoub ◽  
Timothy D Warner ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Human Airway Smooth Muscle ◽  
Endothelin 1 ◽  
Human Airway

scholarly journals In-vitro exposure of guinea pig main bronchi to 2·5 ppm of nitrogen dioxide does not alter airway smooth muscle response

1995 ◽  
Vol 89 (5) ◽  
pp. 323-328 ◽  
Author(s):  
P. Chitano ◽  
R.E. Lucchini ◽  
E. Coser ◽  
A. Papi ◽  
M. Saetta ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Nitrogen Dioxide ◽  
Airway Smooth Muscle ◽  
Muscle Response ◽  
In Vitro Exposure

Role of endothelin-1 in regulating proliferation of cultured rabbit airway smooth muscle cells

1992 ◽  
Vol 263 (3) ◽  
pp. L317-L324 ◽  
Author(s):  
J. P. Noveral ◽  
S. M. Rosenberg ◽  
R. A. Anbar ◽  
N. A. Pawlowski ◽  
M. M. Grunstein
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Phospholipase A2 ◽  
Airway Smooth Muscle ◽  
Pertussis Toxin ◽  
Potential Role ◽  
Cell Number ◽  
Airway Smooth Muscle Cells ◽  
Endothelin 1 ◽  
Mitogenic Action

Increased expression of the potent vasoconstrictor and bronchoactive peptide, endothelin-1 (ET-1), has recently been demonstrated in airway epithelial and endothelial cells of asthmatic patients. To identify its potential role in contributing to airway smooth muscle (ASM) hyperplasia, a characteristic feature of asthmatic airways, the mitogenic action of ET-1 was investigated in cultured rabbit ASM cells. ET-1 elicited significant dose-dependent (10(-12)-10(-6) M) increases in ASM cell number, with a mean potency (i.e., -log mean effective dose) of action of 9.82-log M. ET-1 also acutely stimulated intracellular inositol 1,4,5-trisphosphate accumulation. The latter response was blocked by phospholipase C inhibition with neomycin; however, neomycin had no effect on the promitogenic action of ET-1. By contrast, the ASM cell proliferative response to ET-1 was independently inhibited by pertussis toxin, inhibitors of phospholipase A2, cyclooxygenase, and thromboxane A2 (TxA2) synthesis, as well as blockade of the TxA2 receptor. Moreover, in complementary studies, we found that administration of the stable TxA2 mimetics, carbocyclic TxA2 (CTA2) and U-46619, induced ASM cell proliferation and that ET-1 evoked the release of endogenous TxA2 from the ASM cells. Collectively, these observations provide new evidence that 1) ET-1 is a potent mitogen of ASM cells, 2) the promitogenic effect of ET-1 is associated with activation of a pertussis toxin-sensitive G protein coupled to stimulation of phospholipase A2, and 3) the latter mediates ASM cell proliferation via the release and autocrine mitogenic action of TxA2. The findings support a potential role for ET-1 in mediating the characteristic hyperplasia of ASM in asthma.

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