Am J Physiol Cell Physiol AJP: Regulatory, Integrative and Comparative Physiology
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Am J Physiol Cell Physiol 296: C1034-C1039, 2009. First published March 18, 2009; doi:10.1152/ajpcell.00544.2008
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MUSCLE CELL BIOLOGY AND CELL MOTILITY

CapZ dynamics are altered by endothelin-1 and phenylephrine via PIP2- and PKC-dependent mechanisms

Thomas J. Hartman,1,2 Jody L. Martin,3 R. John Solaro,1,2 Allen M. Samarel,3 and Brenda Russell1,2

1Center For Cardiovascular Research and 2Departments of Physiology and Biophysics, College of Medicine, University of Illinois at Chicago, Chicago; and 3Cardiovascular Institute, Loyola University Medical Center, Maywood, Illinois

Submitted 21 October 2008 ; accepted in final form 14 March 2009

One of the unanswered questions in muscle hypertrophy is how new contractile units are inserted into a stable existing cytoskeletal meshwork. Regulation of actin capping by CapZ may play a role in remodeling processes, therefore, CapZ dynamics are determined during rapid growth of cardiac cells in vitro. Neonatal rat ventricular myocytes were infected with adenovirus expressing green fluorescent protein-CapZ β1 and responded normally to hypertrophic stimuli. CapZ dynamics were analyzed by fluorescence recovery after photobleaching in cultured myocytes treated with endothelin-1 (100 nM) or phenylephrine (10 µM). Recovery by 30 s was greater with endothelin treatment. Analysis 30 min postbleach showed CapZ-infected cells treated with endothelin recovered more completely than controls (77 ± 9% vs. 50 ± 6%, P < 0.001). Similar results were found with phenylephrine (77 ± 5%, P < 0.05). A potential mechanism for phosphatidylinositol bisphosphate (PIP2) mediation of increased CapZ exchange in endothelin- and phenylephrine-treated cells was tested. PIP2 sequestration with neomycin (500 µM) blocked both endothelin- (43 ± 6%, P < 0.001) and phenylephrine (36 ± 4%, P < 0.001)-mediated recovery. The protein kinase C inhibitor chelerythrine chloride (10 µM) also blocked endothelin- (53 ± 10%, P < 0.001) and phenylephrine (42 ± 3%, P < 0.001)-mediated recovery. This study demonstrates for the first time that endothelin and phenylephrine alter CapZ dynamics through PIP2- and PKC-dependent pathways, which might destabilize the existing framework and permit sarcomeric remodelling to proceed.

sarcomere remodeling; heart hypertrophy; thin filament assembly; actin binding; Z-disk


Address for reprint requests and other correspondence: B. Russell, Dept. of Physiology and Biophysics, Univ. of Illinois at Chicago, MC 901, 835 S. Wolcott, Chicago, IL 60612 (e-mail: russell{at}uic.edu)






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