Published online before print May 23, 2005, doi: 10.1161/01.HYP.0000167990.82235.3c
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Hypertension. 2005;46:93.)
© 2005 American Heart Association, Inc.
Original Articles |
Role of the Actin Cytoskeleton in G-Protein–Coupled Receptor Activation of PYK2 and Paxillin in Vascular Smooth Muscle
From the University Department of Medicine, Manchester Royal Infirmary, Oxford Road, Manchester, United Kingdom.
Correspondence to Dr Jacqueline Ohanian, University Department of Medicine, Manchester Royal Infirmary, Oxford Road, Manchester, M13 9WL, UK. E-mail johanian{at}man.ac.uk
Dynamic remodeling of the actin cytoskeleton occurs during agonist-induced smooth muscle contraction. Tyrosine phosphorylation of the adaptor protein paxillin has been implicated in regulation of actin filament formation and force development. We have investigated the role of the actin cytoskeleton in noradrenaline (NA)-induced and endothelin (ET)-induced activation of the calcium-dependent nonreceptor tyrosine kinase PYK2 and subsequent phosphorylation of paxillin in rat small mesenteric arteries. NA and ET induced a rapid and prolonged activation of PYK2, as shown by increased phosphorylation at Y402 and Y881, and a concomitant association of the kinase with a Triton X-100 insoluble membrane (cytoskeleton) compartment. Both agonists also increased phosphorylation of paxillin at Y31 and Y118 with a similar time course as PYK2 phosphorylation, and induced its association with the same membrane compartment as PYK2. Treatment of arteries with cytochalasin D disrupted stress fibers and inhibited NA-induced and ET-induced force in a myosin light chain 20 phosphorylation independent and reversible manner. However, cytochalasin D treatment had no effect on NA-induced and ET-induced phosphorylation of either PYK2 or paxillin but did prevent their association with the TritonX-100 insoluble membrane compartment. These results show that in mesenteric arteries an intact cytoskeleton and force development are not prerequisites for G-protein–coupled receptor–induced activation of PYK2 and paxillin, by tyrosine phosphorylation, in vascular tissue, but are necessary for the translocation of PYK2 and paxillin to the membrane.
Key Words: kinase • mesenteric arteries • phosphorylation
This article has been cited by other articles:
 |
|
 |
|
  L. A. Martinez-Lemus, M. A. Hill, and G. A. Meininger The Plastic Nature of the Vascular Wall: A Continuum of Remodeling Events Contributing to Control of Arteriolar Diameter and Structure Physiology, February 1, 2009; 24(1): 45 - 57. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. R. Kim, C. Gallant, P. C. Leavis, S. J. Gunst, and K. G. Morgan Cytoskeletal remodeling in differentiated vascular smooth muscle is actin isoform dependent and stimulus dependent Am J Physiol Cell Physiol, September 1, 2008; 295(3): C768 - C778. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. J. Gunst and W. Zhang Actin cytoskeletal dynamics in smooth muscle: a new paradigm for the regulation of smooth muscle contraction Am J Physiol Cell Physiol, September 1, 2008; 295(3): C576 - C587. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Srinivasan, S. Forman, R. A. Quinlan, J. Ohanian, and V. Ohanian Regulation of contractility by Hsp27 and Hic-5 in rat mesenteric small arteries Am J Physiol Heart Circ Physiol, February 1, 2008; 294(2): H961 - H969. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. M. Rembold, A. D. Tejani, M. L. Ripley, and S. Han Paxillin phosphorylation, actin polymerization, noise temperature, and the sustained phase of swine carotid artery contraction Am J Physiol Cell Physiol, September 1, 2007; 293(3): C993 - C1002. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. R. Hodges, J. D. Rios, J. Vrouvlianis, I. Ota, D. Zoukhri, and D. A. Dartt Roles of Protein Kinase C, Ca2+, Pyk2, and c-Src in Agonist Activation of Rat Lacrimal Gland p42/p44 MAPK. Invest. Ophthalmol. Vis. Sci., August 1, 2006; 47(8): 3352 - 3359. [Abstract] [Full Text] [PDF]
|
|