Length-dependent changes in contractile dynamics are blunted due to cardiac myosin binding protein-C ablation

Ranganath Mamidi1, Kenneth S Gresham1, Julian E Stelzer1

  • 1Department of Physiology and Biophysics, School of Medicine, Case Western Reserve University Cleveland, OH, USA.

Frontiers in Physiology
|December 19, 2014
PubMed

Insights

Cardiac myosin binding protein-C (cMyBP-C) regulates length-dependent activation (LDA) in the heart. Loss of cMyBP-C impairs the heart's ability to increase force with sarcomere length, affecting cross-bridge dynamics.

Area of Science:

  • Cardiovascular Physiology
  • Muscle Biology
  • Biochemistry

Background:

  • Cardiac contractile function is enhanced by increased sarcomere length (SL), a phenomenon known as length-dependent activation (LDA).
  • Cardiac myosin binding protein-C (cMyBP-C) modulates myosin head positioning, suggesting a role in LDA.
  • The specific contribution of cMyBP-C to cardiac LDA remains unclear.

Purpose of the Study:

  • To investigate the impact of cMyBP-C on length-dependent changes in cardiac muscle function.
  • To elucidate the role of cMyBP-C in regulating cross-bridge kinetics during changes in sarcomere length.

Main Methods:

  • Isometric force, myofilament Ca(2+)-sensitivity (pCa50), and cross-bridge (XB) kinetic parameters (k rel, k df, k tr) were measured in skinned ventricular preparations from wild-type (WT) and cMyBP-C knockout (KO) mice.
  • Experiments were conducted at short (1.9 μm) and long (2.1 μm) sarcomere lengths (SL).
  • Rapid stretch and slack-restretch maneuvers were used to assess dynamic XB behavior.

Main Results:

  • Maximal force was similar between WT and cMyBP-C KO mice.
  • Length-dependent increases in pCa50 were attenuated in KO preparations, particularly at short SL.
  • WT preparations showed length-dependent acceleration of k tr, k rel, and k df, which was absent in KO preparations.

Conclusions:

  • cMyBP-C is crucial for normal length-dependent activation in cardiac muscle.
  • cMyBP-C influences LDA by modulating the dynamic behavior of cardiac cross-bridges in response to changes in sarcomere length.
  • These findings highlight cMyBP-C as a key regulator of cardiac mechanical adaptation.

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