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Myosin heavy chain gene expression in human heart failure
1Department of Molecular, Cellular and Developmental Biology, University of Colorado, Boulder 80309-0347, USA.
The Journal of Clinical Investigation
|December 31, 1997
Summary
Cardiac alpha-myosin heavy chain (MyHC) mRNA is abundant in healthy hearts but significantly reduced in end-stage heart failure. This decrease in alpha-MyHC may explain impaired systolic function in heart failure patients.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Gene Expression
Background:
- Mammalian ventricular myocardium expresses two myosin heavy chain (MyHC) isoforms: alpha and beta.
- Relative MyHC expression correlates with cardiac muscle contractile velocity.
- Pathologic stimuli can induce shifts from alpha- to beta-MyHC in rodent ventricles.
Purpose of the Study:
- To investigate MyHC gene expression in human heart failure.
- To quantify alpha- and beta-MyHC mRNA in nonfailing (NF), donor heart dysfunction (DHD), and failing (F) human hearts.
Main Methods:
- Quantitative analysis of alpha- and beta-MyHC mRNA.
- Comparison of MyHC mRNA levels in left ventricular free walls (LVs) from NF, DHD, and F donor hearts.
Main Results:
- NF and DHD LVs showed surprisingly high relative amounts of alpha-MyHC mRNA (33.3% and 35.4%, respectively).
- Failing LVs exhibited significantly lower alpha-MyHC mRNA levels (2.2%, P < 0.0001) compared to NF and DHD groups.
- No significant difference was observed between NF and DHD groups.
Conclusions:
- A substantial amount of alpha-MyHC mRNA is present in normal human hearts.
- Chronic end-stage heart failure is associated with a significant decrease in alpha-MyHC mRNA expression.
- Reduced alpha-MyHC may contribute to systolic dysfunction in heart failure, suggesting potential therapeutic targets.
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