Nonsynchronous accumulation of α-skeletal actin and β-myosin heavy chain mRNAs during early stages of pressure-overload-induced cardiac hypertrophy demonstrated by in situ hybridization

S. Schiaffino, J. L. Samuel, D. Sassoon, A. M. Lompre, I. Garner, F. Marotte, M. Buckingham, L. Rappaport, K. Schwartz

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Abstract

The development of cardiac hypertrophy secondary to pressure overload is accompanied by isoformic changes of contractile proteins such as myosin and actin. 35S-Labeled complementary RNA (cRNA) probes and in situ hybridization procedures were used for analysis of the regional distribution of newly formed transcripts from α-skeletal actin (α-sk-actin) and β-myosin heavy chain (β-MHC) genes during the early stages of pressure overload. The study was performed in 25-day-old rats submitted to a thoracic aortic stenosis and killed after surgery at times ranging from 4 hours to 3 days. Neither α-sk-actin nor β-MHC messenger RNA (mRNA) was detected in the hearts of normal and sham-operated animals. However, α-sk-actin mRNA accumulated throughout the entire left ventricle as early as 4 hours after aortic stenosis, and by 12 hours was also detected in the left atrium. In contrast, β-MHC mRNA was hardly detectable before day 1, and by days 2-3 was mainly restricted to the inner part of the left ventricle and around the coronary arteries. The absence of spatial and temporal coordination in the accumulation of α-sk-actin and β-MHC mRNAs indicates that different signals and/or regulatory mechanisms are implicated in the induction of the two genes in response to hemodynamic overload.

Original languageEnglish
Pages (from-to)937-948
Number of pages12
JournalCirculation Research
Volume64
Issue number5
DOIs
StatePublished - 1989
Externally publishedYes

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