Role of Rho-kinase in guinea-pig gallbladder smooth muscle contraction

2006 ◽  
Vol 534 (1-3) ◽  
pp. 210-217 ◽  
Author(s):  
Teresa Quinn ◽  
Ronan Feighery ◽  
Alan William Baird
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Muscle Contraction ◽  
Rho Kinase ◽  
Smooth Muscle Contraction

Role of the RhoA/Rho-kinase pathway in the regulation of pulmonary vasoconstrictor function

2010 ◽  
Vol 88 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Bobby D. Nossaman ◽  
Vaughn E. Nossaman ◽  
Subramanyam N. Murthy ◽  
Philip J. Kadowitz
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Calcium Binding ◽  
Rho Kinase ◽  
Smooth Muscle Contraction ◽  
Downstream Effector ◽  
Downstream Effectors ◽  
Vascular Beds ◽  
Kinase Pathway

Calcium is the major intracellular messenger that triggers smooth muscle contraction. The study of calcium-binding proteins, such as calmodulin and its downstream effectors, reveals critical regulation of smooth muscle contraction by protein kinases and phosphatases. Moreover, the small GTP-binding protein RhoA and its downstream effector protein, Rho-kinase, have been shown to play a novel role in the regulation of smooth muscle contraction. Studies have shown that the activation of Rho-kinase is involved in the development of endothelial dysfunction, inflammation, restenosis, and increased vascular tone in a number of cardiovascular disorders. Because inhibitors of this pathway promote vasodilation independent of the mechanism that increases vasoconstrictor tone, it is our hypothesis that Rho-kinase is constitutively active in regulating vasoconstrictor tone in the pulmonary and systemic vascular beds. Studies in the literature suggest that the RhoA/Rho-kinase pathway has an important role in the pathogenesis of pulmonary hypertension.

scholarly journals Role of contractile prostaglandins and Rho-kinase in growth factor-induced airway smooth muscle contraction

2005 ◽  
Vol 6 (1) ◽  
Author(s):  
Dedmer Schaafsma ◽  
Reinoud Gosens ◽  
I Sophie T Bos ◽  
Herman Meurs ◽  
Johan Zaagsma ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Muscle Contraction ◽  
Airway Smooth Muscle ◽  
Rho Kinase ◽  
Smooth Muscle Contraction

Ozone-induced airway hyperresponsiveness: roles of ROCK isoforms

2015 ◽  
Vol 309 (12) ◽  
pp. L1394-L1397 ◽  
Author(s):  
James A. Lambert ◽  
Weifeng Song
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Airway Smooth Muscle ◽  
Airway Hyperresponsiveness ◽  
Rho Kinase ◽  
Smooth Muscle Contraction ◽  
Wild Type ◽  
Epithelial Injury ◽  
Robust Evidence

Acute ozone (O3) inhalation has been shown to cause airway and pulmonary epithelial injury with accompanying inflammation responses. Robust evidence exists that O3 induces airway hyperresponsiveness (AHR) in humans and in animal models. Several pathways exist that culminate in airway smooth muscle contraction, but the mechanism(s) by which O3 elicits AHR are unclear. Here, we review the recent report by Kasahara et al. (Kasahara DI, Mathews JA, Park CY, Cho Y, Hunt G, Wurmbrand AP, Liao JK, Shore SA. Am J Physiol Lung Cell Mol Physiol 309: L736–L746, 2015.) describing the role of two Rho kinase (ROCK) isoforms in O3-induced AHR utilizing a murine haploinsufficiency model. Compared with wild-type (WT) mice, the authors report that ROCK1+/− and ROCK2+/− mice exhibited significantly reduced AHR following acute exposure to O3. Additionally, WT mice treated with fasudil, an FDA-approved ROCK1/2 inhibitor, recapitulated reduction in AHR as seen in ROCK haplotypes. It was suggested that, although the two ROCK isoforms are both induced by Rho, they have different mechanisms by which they mediate O3-induced AHR: ROCK1 via hyaluronan signaling vs. ROCK2 acting downstream of inflammation at the level of airway smooth muscle contraction. These observations provide an important framework to develop novel ROCK-targeting therapies for acute O3-induced AHR.

Contraction of guinea pig ileal smooth muscle by acetyl glyceryl ether phosphorylcholine

1981 ◽  
Vol 241 (3) ◽  
pp. C130-C133 ◽  
Author(s):  
S. R. Findlay ◽  
L. M. Lichtenstein ◽  
D. J. Hanahan ◽  
R. N. Pinckard
Keyword(s):  
Biological Activity ◽  
Smooth Muscle ◽  
Guinea Pig ◽  
Muscle Contraction ◽  
Glyceryl Ether ◽  
Platelet Activating Factor ◽  
Smooth Muscle Contraction

Acetyl glyceryl ether phosphorylcholine (AGEPC) is a chemical that has the biological activity of what was formerly termed platelet-activating factor. We report here that synthetic AGEPC induces the contraction of guinea pig ileal smooth muscle. Antagonists of histamine, acetylcholine, and slow-reacting substances (SRS) do not block AGEPC-induced contraction. These responses were long lasting, resistant to washing, and displayed complete agonist specific desensitization. Histamine- and SRS-induced contractions were unaffected by AGEPC. These studies show that AGEPC has the potential to produce a component of anaphylactically induced smooth muscle contraction.

scholarly journals Allergic sensitization enhances the contribution of Rho-kinase to airway smooth muscle contraction

2004 ◽  
Vol 143 (4) ◽  
pp. 477-484 ◽  
Author(s):  
Dedmer Schaafsma ◽  
Reinoud Gosens ◽  
I Sophie T Bos ◽  
Herman Meurs ◽  
Johan Zaagsma ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Airway Smooth Muscle ◽  
Allergic Sensitization ◽  
Rho Kinase ◽  
Smooth Muscle Contraction

Activation of Rho signaling contributes to lysophosphatidic acid-induced contraction of intact ileal smooth muscle of guinea-pig

2000 ◽  
Vol 78 (9) ◽  
pp. 729-736 ◽  
Author(s):  
Mayumi Mori ◽  
Hiromi Tsushima
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Lysophosphatidic Acid ◽  
Membrane Fraction ◽  
Smooth Muscles ◽  
Rho Kinase ◽  
Specific Inhibitor ◽  
High K ◽  
Rho A

To elucidate the possible role of Rho A/Rho-kinase on lysophosphatidic acid (LPA)-induced contraction in intact guinea-pig ileal smooth muscle, we examined effects of pretreatment with a specific inhibitor of Rho-kinase (Y-27632) on the LPA-induced contraction and MLC20 phosphorylation. In addition, we investigated whether LPA actually elicits an activation of Rho A by studying subcellular distribution of Rho A in unstimulated and stimulated smooth muscles by LPA. LPA induced a less intense, but sustained, contraction compared with ACh, and was accompanied by significant increases in MLC20 phosphorylation. The effects of LPA on tension and MLC20 phosphorylation were inhibited by Y-27632. The ACh-induced contraction, but not increases in MLC20 phosphorylation, was partially inhibited by Y-27632. High K+-induced contraction was unaffected by the inhibitor. LPA stimulated translocation of Rho A from the cytosol to the membrane fraction of the muscle. Translocation of Rho A was also induced by ACh and high K+. These results suggest that LPA-induced contraction of intact ileal smooth muscle is dominated through activation of Rho A and Rho-kinase and subsequent increases in MLC20 phosphorylation.Key words: lysophosphatidic acid, Rho, Rho-kinase, ileal smooth muscle.

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