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Yin Yang 1 represses alpha-myosin heavy chain gene expression in pathologic cardiac hypertrophy

Peter D Mariner1, Stephen W Luckey, Carlin S Long

  • 1Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, CO 80309, USA.

Biochemical and Biophysical Research Communications
|November 30, 2004
PubMed

Insights

This study reveals how Yin Yang 1 (YY1) represses alpha-myosin heavy chain (MyHC) during cardiac hypertrophy. A specific YY1 binding site in the alpha-MyHC promoter is key to this pathological gene expression.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Gene Regulation

Background:

  • Pathological cardiac hypertrophy involves altered gene expression, including reduced alpha-myosin heavy chain (MyHC).
  • Understanding the regulatory mechanisms behind MyHC repression is crucial for developing therapeutic strategies.

Purpose of the Study:

  • To elucidate the mechanism by which alpha-myosin heavy chain (MyHC) expression is repressed during pathological cardiac hypertrophy.
  • To identify the role of the transcription factor Yin Yang 1 (YY1) in this process.

Main Methods:

  • Utilized neonatal rat ventricular myocytes to study gene expression.
  • Performed promoter analysis, including mutation of YY1 binding sites.
  • Assessed alpha-MyHC mRNA and protein levels.

Main Results:

  • Demonstrated that Yin Yang 1 (YY1) significantly decreases alpha-myosin heavy chain (MyHC) mRNA and protein.
  • Showed that mutating YY1 binding sites in the alpha-MyHC promoter increases its activity.
  • Identified a specific YY1 binding site (-94bp) essential for repression by phorbol esters.

Conclusions:

  • YY1 is a key repressor of alpha-MyHC during pathological cardiac hypertrophy.
  • A single critical YY1 binding site mediates the repression of alpha-MyHC expression.
  • This finding reveals a unique mechanism for regulating MyHC in cardiac hypertrophy.

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