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Updated: Apr 19, 2026

Assessment of Myofilament Ca2+ Sensitivity Underlying Cardiac Excitation-contraction Coupling
Published on: August 1, 2016
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.
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.
Abstract:
Enhanced cardiac contractile function with increased sarcomere length (SL) is, in part, mediated by a decrease in the radial distance between myosin heads and actin. The radial disposition of myosin heads relative to actin is modulated by cardiac myosin binding protein-C (cMyBP-C), suggesting that cMyBP-C contributes to the length-dependent activation (LDA) in the myocardium. However, the precise roles of cMyBP-C in modulating cardiac LDA are unclear. To determine the impact of cMyBP-C on LDA, we measured isometric force, myofilament Ca(2+)-sensitivity (pCa50) and length-dependent changes in kinetic parameters of cross-bridge (XB) relaxation (k rel), and recruitment (k df) due to rapid stretch, as well as the rate of force redevelopment (k tr) in response to a large slack-restretch maneuver in skinned ventricular multicellular preparations isolated from the hearts of wild-type (WT) and cMyBP-C knockout (KO) mice, at SL's 1.9 μm or 2.1 μm. Our results show that maximal force was not significantly different between KO and WT preparations but length-dependent increase in pCa50 was attenuated in the KO preparations. pCa50 was not significantly different between WT and KO preparations at long SL (5.82 ± 0.02 in WT vs. 5.87 ± 0.02 in KO), whereas pCa50 was significantly different between WT and KO preparations at short SL (5.71 ± 0.02 in WT vs. 5.80 ± 0.01 in KO; p < 0.05). The k tr, measured at half-maximal Ca(2+)-activation, was significantly accelerated at short SL in WT preparations (8.74 ± 0.56 s(-1) at 1.9 μm vs. 5.71 ± 0.40 s(-1) at 2.1 μm, p < 0.05). Furthermore, k rel and k df were accelerated by 32% and 50%, respectively at short SL in WT preparations. In contrast, k tr was not altered by changes in SL in KO preparations (8.03 ± 0.54 s(-1) at 1.9 μm vs. 8.90 ± 0.37 s(-1) at 2.1 μm). Similarly, KO preparations did not exhibit length-dependent changes in k rel and k df. Collectively, our data implicate cMyBP-C as an important regulator of LDA via its impact on dynamic XB behavior due to changes in SL.
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