The dynamic role of cardiac myosin binding protein-C during ischemia.

Cardiac myosin binding protein C (cMyBP-C) is a myofibrillar protein important for normal myocardial contractility and stability. In mutated form it can cause cardiomyopathy and heart failure. cMyBP-C appears to have separate regions for different functions.

Phosphorylation of contractile proteins in response to alpha- and beta-adrenergic stimulation in neonatal cardiomyocytes.

alpha- and beta-Adrenergic receptor agonists induce an inotropic response in the adult heart by promoting the phosphorylation of several regulatory proteins, including myosin-binding protein C (MyBP-C), cardiac troponin I (cTnI), and phospholamban (PLB). However, the adrenergic-induced phosphorylation of these proteins has not been characterized in the developing heart. Accordingly, we evaluated MyBP-C, cTnI, and PLB phosphorylation in cultured neonatal rat cardiomyocytes (NRCMs) after alpha- and beta-receptor activation with phenylephrine and isoproterenol.

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

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.

Infarct resorption, compensatory hypertrophy, and differing patterns of ventricular remodeling following myocardial infarctions of varying size.

Objectives: We sought to identify advantages of contrast-enhanced magnetic resonance imaging (MRI) in studying postinfarction ventricular remodeling.

Background: Although sequential measurements of ventricular volumes, internal dimensions, and total ventricular mass have provided important insights into postinfarction left ventricular remodeling, it has not been possible to define serial, directionally opposite changes in resorption of infarcted tissue and hypertrophy of viable myocardium and effects of these changes on commonly used indices of remodeling.

Methods: Using gadolinium-enhanced MRI, the time course and geometry of changes in infarcted and noninfarcted regions were assessed serially in dogs subjected to coronary occlusion for 45 min, 90 min, or permanently.

HSC73-tubulin complex formation during low-flow ischemia in the canine myocardium.

Canine myocardium was exposed to bouts of low-flow ischemia to identify the interactions that develop between the microtubule-based cytoskeleton and the heat shock protein 70 (HSP70) family of heat shock proteins in viable cardiomyocytes. "Moderate" or "severe" low-flow ischemia was produced in chronically instrumented dogs by reducing circumflex coronary flow by 50% for 2 h or by 75% for 5 h followed by reperfusion for 2 and 24 h, respectively. Electron and immunofluorescence microscopy demonstrated either partial or nearly complete depolymerization of the intermyofibrillar microtubules in areas of myofibril disruption and partial dissolution of the perinuclear microtubule girdle.