title: Myosin-binding protein C phosphorylation, myofibril structure, and contractile function during low-flow ischemia.
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.
  
  
  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.
authors.affiliation: Feinberg Cardiovascular Research Institute, Tarry 12-733, Feinberg School of Medicine, Northwestern University, 303 E Chicago Ave, Chicago, IL 60611-3008, USA. r-decker@northwestern.edu
authors.forename: Robert S
authors.initials: RS
authors.lastname: Decker
authors.forename: Marlene L
authors.initials: ML
authors.lastname: Decker
authors.forename: Irina
authors.initials: I
authors.lastname: Kulikovskaya
authors.forename: Sakie
authors.initials: S
authors.lastname: Nakamura
authors.forename: Daniel C
authors.initials: DC
authors.lastname: Lee
authors.forename: Kathleen
authors.initials: K
authors.lastname: Harris
authors.forename: Francis J
authors.initials: FJ
authors.lastname: Klocke
authors.forename: Saul
authors.initials: S
authors.lastname: Winegrad
mesh_terms: D000199:Actins / Q000378:metabolism; D000205:Actomyosin / Q000378:metabolism; D000818:Animals; D002352:Carrier Proteins / Q000378:metabolism*; D004285:Dogs; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D015425:Myocardial Reperfusion; D009210:Myofibrils / Q000648:ultrastructure*; D009218:Myosins / Q000378:metabolism; D010766:Phosphorylation; D000099163:Myosin Binding Protein C
chemical_list: D000199:Actins; D000205:Actomyosin; D002352:Carrier Proteins; D009218:Myosins; D000099163:Myosin Binding Protein C