title: Alterations in myosin heavy chain isoform gene expression during the transition from compensatory hypertrophy to congestive heart failure in rats.
abstract: OBJECTIVE
  To explore the molecular mechanism underlying the decreased velocity of tension rise in rat myocardium during congestive heart failure (CHF) and left ventricular hypertrophy (LVH) induced by aortic stenosis.
  
  
  METHODS
  The maximum velocity of tension rise (+dT/dtmax) was measured in left ventricular papillary muscle and the mRNA level of myosin heavy chain (MHC) isoforms in the left ventricle were detected by Northern blot analysis.
  
  
  RESULTS
  The value of +dT/dtmax in CHF and LVH group were 64.17% and 37.15% lower than sham-operated controls (Sham) (P < 0.01); values in the CHF group were 42.99% lower than that of LVH (P < 0.01). The level of alpha-MHC mRNA in LVH was not different from that of the Sham (P > 0.05), but decreased significantly in CHF to 42.3% of Sham and 56.1% of LVH (P < 0.01). The level of beta-MHC mRNA was up-regulated by 88.3% (P < 0.01) in LVH compared with Sham and the level of beta-MHC in CHF was 1.5-fold and 3.7-fold higher than that in LVH and Sham respectively (P < 0.01). The ratio of alpha-MHC/beta-MHC mRNA in LVH and CHF decreased to 42.4% and 9.8% respectively of the value in Sham (P < 0.01). Correlation between alpha-MHC/beta-MHC mRNA level and +dT/dtmax was analyzed which showed that these values were positively correlated with a correlation coefficient of 0.875 (P < 0.01).
  
  
  CONCLUSIONS
  The decreased ratio of alpha-MHC/beta-MHC mRNA was the major molecular mechanism underlying the decreased +dT/dtmax in CHF and LVH myocardium. The decreased ratio of alpha-MHC/beta-MHC mRNA in LVH was mainly due to the up regulation of beta-MHC mRNA while in CHF both down regulation of alpha-MHC and up regulation of beta-MHC were involved.
authors.affiliation: Laboratory of Molecular Pharmacology, Hunan Medical University, Changsha 410078, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Huang
authors.forename: H
authors.initials: H
authors.lastname: Liu
authors.forename: Y
authors.initials: Y
authors.lastname: Li
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D015870:Gene Expression; D006333:Heart Failure / Q000235:genetics / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000235:genetics / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000502:physiology; D009200:Myocardial Contraction / Q000502:physiology; D018995:Myosin Heavy Chains / Q000235:genetics*; D010210:Papillary Muscles / Q000503:physiopathology; D020033:Protein Isoforms / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar
chemical_list: D020033:Protein Isoforms; D012333:RNA, Messenger; D018995:Myosin Heavy Chains