title: Nonsynchronous accumulation of alpha-skeletal actin and beta-myosin heavy chain mRNAs during early stages of pressure-overload--induced cardiac hypertrophy demonstrated by in situ hybridization.
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 alpha-skeletal actin (alpha-sk-actin) and beta-myosin heavy chain (beta-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 alpha-sk-actin nor beta-MHC messenger RNA (mRNA) was detected in the hearts of normal and sham-operated animals. However, alpha-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, beta-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 alpha-sk-actin and beta-MHC mRNAs indicates that different signals and/or regulatory mechanisms are implicated in the induction of the two genes in response to hemodynamic overload.
authors.affiliation: INSERM U127, Université Paris VII, Hôpital Lariboisière, Paris, France.
authors.forename: S
authors.initials: S
authors.lastname: Schiaffino
authors.forename: J L
authors.initials: JL
authors.lastname: Samuel
authors.forename: D
authors.initials: D
authors.lastname: Sassoon
authors.forename: A M
authors.initials: AM
authors.lastname: Lompré
authors.forename: I
authors.initials: I
authors.lastname: Garner
authors.forename: F
authors.initials: F
authors.lastname: Marotte
authors.forename: M
authors.initials: M
authors.lastname: Buckingham
authors.forename: L
authors.initials: L
authors.lastname: Rappaport
authors.forename: K
authors.initials: K
authors.lastname: Schwartz
mesh_terms: D000199:Actins / Q000032:analysis* / Q000235:genetics; D000818:Animals; D001024:Aortic Valve Stenosis / Q000150:complications / Q000503:physiopathology; D006332:Cardiomegaly / Q000209:etiology / Q000378:metabolism*; D005260:Female; D006439:Hemodynamics; D009218:Myosins / Q000032:analysis* / Q000235:genetics; D009693:Nucleic Acid Hybridization; D015347:RNA Probes / Q000032:analysis; D012333:RNA, Messenger / Q000032:analysis*; D051381:Rats
chemical_list: D000199:Actins; D015347:RNA Probes; D012333:RNA, Messenger; D009218:Myosins