Localization of Changes inβ-actin Expression in Remodeled Canine Myocardium

Localization of Changes inβ-actin Expression in Remodeled Canine Myocardium

β-actin is a cytoskeletal protein that has been implicated as a potentially important mediator of the growth, signaling, migration, and remodeling of cells. Beta-actin is upregulated in remodeling myocardium in response to either pressure or volume overload. The cellular localization of this respons...

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Bibliographic Details
Published in:Journal of molecular and cellular cardiology Vol. 31; no. 4; pp. 751 - 760
Main Authors: Tian, Bin, Carlyle, Wenda C., Weigold, W.Guy, McDonald, Kenneth M., Judd, Dianne L., Toher, Cynthia A., Homans, David C., Cohn, Jay N.
Format: Journal Article
Language:English
Published: England Elsevier Ltd 01-04-1999
Subjects:
Actins - metabolism
Animals
Beta-actin
Canine
Cardiac interstitium
Cytoskeleton
Dogs
Endothelial
Endothelium - metabolism
Hypertrophy
Immunohistochemistry
Mitral Valve Insufficiency - metabolism
Mitral Valve Insufficiency - pathology
Myocardium - metabolism
Myocardium - pathology
Remodeling
Ventricular Dysfunction, Left - metabolism
Ventricular Dysfunction, Left - pathology
von Willebrand Factor - metabolism
Endothelial
Beta-actin
Cytoskeleton
Cardiac interstitium
Remodeling
Canine
Hypertrophy
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Summary:β-actin is a cytoskeletal protein that has been implicated as a potentially important mediator of the growth, signaling, migration, and remodeling of cells. Beta-actin is upregulated in remodeling myocardium in response to either pressure or volume overload. The cellular localization of this response has, however, not been determined and is a necessary first step to begin to clarify the role ofβ-actin in myocardial remodeling. Here we demonstrate thatβ-actin protein was confined primarily to the cardiac interstitium using immunofluorescent and immunohistochemical staining. Furthermore, both staining and immunoblotting showed markedly increasedβ-actin protein in myocardium within 24 h of either regional left ventricular damage or chronic volume overload. More importantly, this increase persisted up to 90 days in both models. Double staining showed co-localization ofβ-actin protein and von Willebrand factor, a specific endothelial cell marker. These results suggest that increasedβ-actin expression predominantly localized in cardiac interstitial cells, including endothelial cells. The increasedβ-actin could be due to either proliferation of the interstitial cells or upregulation of theβ-actin gene.
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ISSN:0022-2828
1095-8584
DOI:10.1006/jmcc.1998.0909