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Sexually dimorphic myofilament function and cardiac troponin I phosphospecies distribution in hypertrophic

Laurel A K McKee1, Hao Chen, Jessica A Regan

  • 1Department of Physiology, Sarver Molecular Cardiovascular Research Program, University of Arizona, 1501 N. Campbell Ave., Tucson, AZ 85724, USA.

Archives of Biochemistry and Biophysics
|January 29, 2013
PubMed

Insights

Hypertrophic cardiomyopathy (HCM) progresses differently in male and female mice. Altered myofilament function in female HCM mice contributes to sex-specific cardiac disease development.

Area of Science:

  • Cardiovascular Biology
  • Muscle Physiology
  • Sex Differences in Disease

Background:

  • Pathological progression of hypertrophic cardiomyopathy (HCM) exhibits sexual dimorphism.
  • Male HCM mice show cardiac disease indicators earlier than female HCM mice.

Purpose of the Study:

  • To investigate if alterations in myofilament function contribute to the sex dimorphism in HCM disease development.
  • To examine sex-specific differences in Ca(2+)-sensitive tension and sarcomeric protein expression in HCM mice.

Main Methods:

  • Assessed Ca(2+)-sensitive tension development in demembranated cardiac trabeculae from male and female HCM mice.
  • Quantified protein expression of SERCA2a, β-MyHC, and cardiac troponin T (cTnT) phosphorylation.
  • Analyzed cardiac troponin I (cTnI) phosphospecies distribution using phosphate-affinity SDS-PAGE.

Main Results:

  • Female HCM trabeculae exhibited higher Ca(2+) sensitivity compared to wild-type (WT) and male HCM trabeculae.
  • Female HCM hearts showed elevated SERCA2a and β-MyHC.
  • Male HCM hearts had elevated β-MyHC but reduced cTnT phosphorylation; cTnI phosphospecies distribution varied by sex and HCM status.

Conclusions:

  • Female and male HCM mice display sex-dimorphic myofilament function.
  • These functional differences are associated with sex- and HCM-dependent alterations in sarcomeric protein expression and cTnI phosphorylation patterns.

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