beta-actin is a cytoskeletal protein that has been implicated as a potentia
lly 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 resp
onse has, however, not been determined and is a necessary first step to beg
in to clarify the role of beta-actin in myocardial remodeling. Here we demo
nstrate that beta-actin protein was confined primarily to the cardiac inter
stitium using immunofluorescent and immunohistochemical staining. Furthermo
re, both staining and immunoblotting showed markedly increased beta-actin p
rotein in myocardium within 24 h of either regional left Ventricular damage
or chronic volume overload. More importantly, this increase persisted up t
o 90 days in both models. Double staining showed co-localization of beta-ac
tin protein and non Willebrand factor, a specific endothelial cell marker.
These results suggest that increased beta-actin expression predominantly lo
calized in cardiac interstitial cells, including endothelial cells. The inc
reased beta-actin could be due to either proliferation of the interstitial
cells or upregulation of the beta-actin gene, (C) 1999 Academic Press.