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 of β-actin in myocardial remodeling. Here we demonstrate that β-actin protein was confined primarily to the cardiac interstitium using immunofluorescent and immunohistochemical staining. Furthermore, both staining and immunoblotting showed markedly increased β-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 β-actin protein and von Willebrand factor, a specific endothelial cell marker. These results suggest that increased β-actin expression predominantly localized in cardiac interstitial cells, including endothelial cells. The increased β-actin could be due to either proliferation of the interstitial cells or upregulation of the β-actin gene.
Bibliographical noteFunding Information:
The authors would like to express their sincere appreciation for the excellent assistance they received from Kathleen Hauer, Melinda Hartman, Tracy Elbers, Scott McKnite and Jerald Sedgewick. Grant support was provided by Bayer Corporation and the American Heart Association, Minnesota Affiliate.
- Cardiac interstitium