CHANGES IN BETA-ACTIN MESSENGER-RNA EXPRESSION IN REMODELING CANINE MYOCARDIUM

Beta-actin, a cytoskeletal protein important in the maintenance of cyt oarchitecture, has long been thought to be expressed constitutively in myocardial tissue. As such, beta-actin mRNA has been used as a contro l gene in a wide range of experiments. However, we have uncovered cons istent changes in beta-actin mRNA expression in canine myocardium remo deling as a result of insult to the left ventricle. The experimental c anine models used were either DC shock damage to the left ventricle or volume overload resulting from severe mitral regurgitation. The remod eling process in both canine models is characterized by an increase in left ventricular mass. PCR amplification using primers designed to se lectively amplify the 3' end and a portion of the 3' untranslated regi on of beta-actin mRNA resulted in the generation of a 297 base pair pr oduct predominant only in normal canine myocardium and a 472 base pair product that became increasingly prominent from 1 to 30 days after DC shock damage to the left ventricle and from 10 to 90 days after creat ion of mitral regurgitation. Northern analysis showed a three-fold inc rease in beta-actin mRNA after either DC shock or creation of mitral r egurgitation. Western analysis revealed an early increase in beta-acti n protein followed by an apparent decrease to below baseline levels. T hese observations suggest that changes in beta-actin mRNA expression a ccompany the structural alterations that occur in response to myocardi al damage. Whether or not the changes in beta-actin mRNA expression pl ay a role in mediating these structural alterations remains to be dete rmined. (C) 1996 Academic Press Limited