Myosin-binding protein C phosphorylation, myofibril structure, and contractile function during low-flow ischemia.

Robert S Decker; Marlene L Decker; Irina Kulikovskaya; Sakie Nakamura; Daniel C Lee; Kathleen Harris; Francis J Klocke; Saul Winegrad

doi:10.1161/01.cir.0000155609.95618.75

PubMed · 15699252

Myosin-binding protein C phosphorylation, myofibril structure, and contractile function during low-flow ischemia.

Robert S Decker·Marlene L Decker·Irina Kulikovskaya·Sakie Nakamura·Daniel C Lee·Kathleen Harris·Francis J Klocke·Saul Winegrad

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Abstract

BACKGROUND: Contractile dysfunction develops in the chronically instrumented canine myocardium after bouts of low-flow ischemia and persists after reperfusion. The objective of this study is to identify whether changes in the phosphorylation state of myosin-binding protein C (MyBP-C) are a potential cause of dysfunction. METHODS AND RESULTS: During low-flow ischemia, MyBP-C is dephosphorylated, and the number of actomyosin cross-bridges in the central core of the sarcomere decreases as thick filaments dissemble from the periphery of the myofibril. During reperfusion, MyBP-C remains dephosphorylated, and its degradation is accelerated. CONCLUSIONS: Dephosphorylation of MyBP-C may initiate changes in myofibril thick filament structure that decrease the interaction of myosin heads with actin thin filaments. Limiting the formation of actomyosin cross-bridges may contribute to the contractile dysfunction that is apparent after low-flow ischemia. Breakdown of MyBP-C during reperfusion may prolong myocardial stunning.

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Actins Actomyosin Animals Carrier Proteins Dogs Myocardial Contraction Myocardial Ischemia Myocardial Reperfusion Myofibrils Myosins Phosphorylation Myosin Binding Protein C Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

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Robert S Decker, Marlene L Decker, Irina Kulikovskaya, Sakie Nakamura, Daniel C Lee, Kathleen Harris, Francis J Klocke, Saul Winegrad. 2005-02-07. Myosin-binding protein C phosphorylation, myofibril structure, and contractile function during low-flow ischemia.. https://doi.org/10.1161/01.cir.0000155609.95618.75

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