α-Skeletal actin is associated with increased contractility in the mouse heart

Timothy Hewett, Ingrid L. Grupp, Gunter Grupp, Jeffrey Robbins

Research output: Contribution to journalArticle

114 Scopus citations

Abstract

BALB/c mice express abnormally high levels of α-skeletal actin in the heart, which may be related to a duplication in the promoter of the α- cardiac actin gene. To evaluate the effects of overexpression of the α- skeletal actin isoform on cardiac contractile function, we studied these mice using the isolated perfused work-performing murine heart model and measured actin isoform expression in the same hearts. We quantified myocardial contractility from the maximum rate of contraction (+dP/dt) and time to peak pressure and relaxation from -dP/dt and time to half relaxation of left intraventricular pressure. Dot blots of total RNA hybridized against oligonucleotide sequences specific for either α-skeletal or α-cardiac actin mRNA showed that increased levels of α-skeletal actin RNA correlated significantly with increased contractility of hearts from the BALB/c mice (r=.80, n=15, P<.001). The present study demonstrates a significant functional correlation between α-actin isoform content and cardiac contractile function and also that α-skeletal actin may promote an increased contractile function in the heart compared with α-cardiac actin.

Original languageEnglish (US)
Pages (from-to)740-746
Number of pages7
JournalCirculation Research
Volume74
Issue number4
StatePublished - Apr 1994
Externally publishedYes

Keywords

  • α-actin
  • mouse hearts
  • myocardial function

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

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