© 2000 American Heart Association, Inc.
Vascular Biology |
Cyclic GMP–Dependent Protein Kinase Expression in Coronary Arterial Smooth Muscle in Response to Balloon Catheter Injury
From the Departments of Pathology (P.G.A., N.J.B., T.L.C., T.M.L.) and Medicine (M.L.), School of Medicine, University of Alabama at Birmingham, and the Department of Pharmacology (D.B.M.), School of Medicine, Tulane University, New Orleans, La.
Correspondence to Thomas M. Lincoln, PhD, Department of Pathology, Division of Molecular and Cellular Pathology, University of Alabama at Birmingham, 1670 University Blvd, Birmingham, AL 35294-0019. E-mail lincoln{at}uab.edu
Abstract—Arterial smooth muscle cells undergo phenotypic and proliferative changes in response to balloon catheter injury. Nitric oxide (NO) and cGMP have been implicated in the inhibition of vascular smooth muscle cell proliferation and phenotypic modulation in cultured-cell studies. We have examined the expression of the major cGMP receptor protein in smooth muscle, cGMP-dependent protein kinase I (PKG), in response to balloon catheter injury in the swine coronary artery. On injury, there was a transient decrease in the expression of PKG in neointimal smooth muscle cells when compared with medial smooth muscle cells. The decrease in PKG expression was observed in the population of proliferating cells expressing the extracellular matrix protein osteopontin but not in cells present in the uninjured portion of the media. Coincident with the suppression of PKG expression in neointimal cells after injury, there was a marked increase in the expression of type II NO synthase (inducible NOS [iNOS], NOS-II) in the neointimal cells. These results suggest that PKG expression is transiently reduced in response to injury in the population of coronary arterial smooth muscle cells that are actively proliferating and producing extracellular matrix proteins. The reduction in PKG expression is also correlated temporally with increases in inflammatory activity in the injured vessels as assessed by iNOS expression. Coupled with our current knowledge regarding the role of PKG in the regulation of cultured cell phenotypes, these results imply that PKG may also regulate phenotypic modulation of vascular smooth muscle cells in vivo as well.
Key Words: nitric oxide • restenosis • cGMP • vascular smooth muscle • phenotype
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