Localization of changes in beta-actin expression in remodeled canine myocardium.
Beta-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 of beta-actin in myocardial remodeling. Here we demonstrate that beta -actin protein was confined primarily to the cardiac interstitium using immunofluorescent and immunohistochemical staining. Furthermore, both staining and immunoblotting showed markedly increased beta-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 of beta-actin protein and von Willebrand factor, a specific endothelial cell marker. These results suggest that increased beta-actin expression predominantly localized in cardiac interstitial cells, including endothelial cells. The increased beta-actin could be due to either proliferation of the interstitial cells or upregulation of the beta-actin gene.
D000199:Actins / Q000378:metabolism*; D000818:Animals; D004285:Dogs; D004727:Endothelium / Q000378:metabolism; D007150:Immunohistochemistry; D008944:Mitral Valve Insufficiency / Q000378:metabolism / Q000473:pathology; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D018487:Ventricular Dysfunction, Left / Q000378:metabolism / Q000473:pathology; D014841:von Willebrand Factor / Q000378:metabolism