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. ^-Labeled complementary RNA (cRNA) probes and hi situ hybridization procedures were used for analysis of the regional distribution of newly formed transcripts from a-skeletal actin (a-sk-actin) and 0-myosin heavy chain (fi-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 a-sk-actin nor fi-MHC messenger RNA (mRNA) was detected in the hearts of normal and sham-operated animals. However, a-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, /3-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 a-sk-actin and fi-MHC mRNAs indicates that different signals and/or regulatory mechanisms are implicated in the induction of the two genes hi response to hemodynamic overload. (Circulation Research 1989;64:937-948) C ardiac hypertrophy secondary to pressure overload is accompanied in the rat heart by induction of two contractile protein isogenes, /3-myosin heavy chain (fi-MHC) and askeletal actin (a-sk-actin), which are expressed during early developmental stages but are not expressed or are expressed at very low levels in the normal adult animal (for a review, see Swynghedauw 1 ). In rats, fi-MHC messenger RNAs (mRNAs) and a-skactin mRNAs accumulate in the left ventricle within

Species‐specific differences of myosin content in the developing cardiac chambers of fish, birds, and mammals

“…This highly conserved homology is also shared with skeletal muscle-specific isoforms at both amino acid and nucleotide sequences (Habets et al, 1999 (Melton et al, 1984). Complementary RNA probes against chicken AMHC1 (Yutzley et al, 1994), chicken VMHC1 (Bishaba and Bader, 1991), rat ␣MyHC (Schiaffino et al, 1989;Boheler et al, 1992) and rat ␤MyHC (Boheler et al, 1992) mRNAs were used as positive controls on the hybridisation assays in chicken and mouse embryos. Hybridisation conditions were as described elsewhere (Moorman et al, 1995Franco et al, 2001).…”

Cellular Distribution of Ca 2+ Pumps and Ca 2+ Release Channels in Rat Cardiac Hypertrophy Induced by Aortic Stenosis

“…33 One day, 5 days, and 1 month later, operated and sham-operated (Sh) animals were killed by pentobarbital injection and the hearts were dissected and weighed. Animals did not have dyspnea, pulmonary edema, or ascites, and the weight of right ventricle was unchanged indicating that they did not develop cardiac failure.…”

“…All probes were diluted to a final specific activity of about 60 000 cpm/mL as described. 1,33 Immunolabeling SERCA 2a polyclonal antibodies (gift from Dr F. Wuytack) were as described previously. 36 The anti-chicken pectoralis RyR monoclonal antibody (MA3-925) was obtained from ABR, Inc (Golden, Colorado).…”

“…Because previous qualitative analysis 33 has clearly demonstrated that the response of ventricular myocytes to pressure overload is heterogeneous and not spatially coordinated, we investigated the cellular distribution of Ca 2ϩ pumps and Ca 2ϩ release channels during development of rat cardiac hypertrophy secondary to coarctation of the ascending aorta, a model where SERCA 2 and RyR2 gene expression were undoubtedly reduced.…”

Cardiac myocytes as targets for the action of peptide growth factors.

“…As a result of their lesser ATPase activity, J3MHCs are thought to produce greater economy of contraction but diminished myocardial contractility. 91 In contrast, any anatomic or physiological consequences of fetal actin expression are unproven. Thus, we423 and others45 have proposed that recapitulation of the fetal program by altered load might be indicative of shared regulatory elements rather than adaptation per se.…”