Changes in β-actin mRNA expression in remodeling canine myocardium

Wenda C. Carlyle, Cynthia A. Toher, Jonathan R. Vandervelde, Kenneth M. McDonald, David C. Homans, Jay N. Cohn

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31 Scopus citations


Beta-actin, a cytoskeletal protein important in the maintenance of cytoarchitecture, has long been thought to be expressed constitutively in myocardial tissue. As such, β-actin mRNA has been used as a control gene in a wide range of experiments. However, we have uncovered consistent changes in β-actin mRNA expression in canine myocardium remodeling as a result of insult to the left ventricle. The experimental canine models used were either DC shock damage to the left ventricle or volume overload resulting from severe mitral regurgitation. The remodeling process in both canine models is characterized by an increase in left ventricular mass. PCR amplification using primers designed to selectively amplify the 3' end and a portion of the 3' untranslated region of β-actin mRNA resulted in the generation of a 297 base pair product 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 creation of mitral regurgitation. Northern analysis showed a three-fold increase in β-actin mRNA after either DC shock or creation of mitral regurgitation. Western analysis revealed an early increase in β-actin protein followed by an apparent decrease to below baseline levels. These observations suggest that changes in β-actin mRNA expression accompany the structural alterations that occur in response to myocardial damage. Whether or not the changes in β-actin mRNA expression play a role in mediating these structural alterations remains to be determined.

Original languageEnglish (US)
Pages (from-to)53-63
Number of pages11
JournalJournal of Molecular and Cellular Cardiology
Issue number1
StatePublished - Jan 8 1996

Bibliographical note

Funding Information:
The authors wish to thank Dr Robert Bache for his support and guidance. They also wish to express their appreciation for technical assistance from Lynn Hartman, Kate Hauer, Tracy Elbers, Todd Pavek, Melanie Crampton, Sara Herrlinger and Todd Parrish. This study was supported in part by Program Project Grant (PO132427) and research grant (021872) from the National Heart, Lung and Blood Institute, Minnesota American Heart Association Grant-in-aid, a gift from the Pharmaceutical Division of Miles, Inc., and the Bristol-Myers Squibb Cardiovascular Research Grant Award.


  • Canine gene expression
  • Cytoskeletal protein
  • DC shock
  • Mitral regurgitation
  • Ventricular remodeling
  • β-actin


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