calmodulin/enfarktüs

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[ATPase activity of the heart microsomes, the regulation of calcium transport in the microsomes and the calmodulin content in experimental myocardial infarct].

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Calmodulin and cAMP were demonstrated to have no stimulating effect on Ca2+ transport in the sarcoplasmic reticulum of the dog heart in experimental myocardial infarction as compared to that in the uninvolved myocardium (control). Introduction to the incubation medium of exogenous protein kinase in

DY-9760e, a novel calmodulin antagonist, reduces infarction after permanent focal cerebral ischemia in rats.

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DY-9760e (3-[2-[4-(3-chloro-2-methylphenyl)-1-piperazinyl]ethyl]-5,6-dimethoxy-1-(4-imidazolylmethyl)-1H-indazole dihydrochloride 3.5 hydrate), a novel calmodulin antagonist, provides effective protection against Ca(2+) ionophore-induced cytotoxicity and brain injury induced by transient focal

Post-ischemic administration of DY-9760e, a novel calmodulin antagonist, reduced infarct volume in the permanent focal ischemia model of spontaneously hypertensive rat.

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We assessed the effect of a novel calmodulin antagonist, DY-9760e (3-[2-[4-(3-chloro-2-methylphenyl)-1-piperazinyl]ethyl]-5,6-dimethoxy-1-(4-imidazolylmethyl)-1H-indazole dihydrochloride 3.5 hydrate) in a spontaneously hypertensive rat (SHR) permanent focal cerebral ischemia. In experiment I, the

Oxidized calmodulin kinase II regulates conduction following myocardial infarction: a computational analysis.

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Calmodulin kinase II (CaMKII) mediates critical signaling pathways responsible for divergent functions in the heart including calcium cycling, hypertrophy and apoptosis. Dysfunction in the CaMKII signaling pathway occurs in heart disease and is associated with increased susceptibility to

Wenxin-Keli Regulates the Calcium/Calmodulin-Dependent Protein Kinase II Signal Transduction Pathway and Inhibits Cardiac Arrhythmia in Rats with Myocardial Infarction.

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Wenxin-Keli (WXKL) is a Chinese herbal compound reported to be of benefit in the treatment of cardiac arrhythmia, cardiac inflammation, and heart failure. Amiodarone is a noncompetitive inhibitor of the α - and β -adrenergic receptors and prevents calcium influx in the slow-response cells of the

Involvement of the dual-specificity tyrosine phosphorylation-regulated kinase 1A-alternative splicing factor-calcium/calmodulin-dependent protein kinase IIδ signaling pathway in myocardial infarction-induced heart failure of rats.

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BACKGROUND Alternative splicing factor (ASF)-regulated alternative splicing of calcium/calmodulin-dependent protein kinase IIδ (CaMKIIδ) plays an important role in pathologic cardiac remodeling. ASF can be phosphorylated by dual-specificity tyrosine phosphorylation-regulated kinase 1A (Dyrk1A). This

Ablation of PLN rescues reperfusion arrhythmias but exacerbates myocardium infarction in hearts with Ca2+/calmodulin kinase II constitutive phosphorylation of ryanodine receptors.

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UNASSIGNED Abnormal Ca2+ release from the sarcoplasmic reticulum (SR), associated with CaMKII-dependent phosphorylation of RyR2 at Ser2814, has consistently been linked to arrhythmogenesis and ischemia/reperfusion-induced cell death. In contrast, the role played by SR Ca2+ uptake under these stress

A role for calcium/calmodulin-dependent protein kinase II in cardiac disease and arrhythmia.

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More than 20 years have passed since the discovery that a collection of specific calcium/calmodulin-dependent phosphorylation events is the result of a single multifunctional kinase. Since that time, we have learned a great deal about this multifunctional and ubiquitous kinase, known today as

Protective effect of calmodulin inhibitors on reperfusion injury.

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Activation of an intracellular calcium-calmodulin complex may play an important role in myocardial injury induced by ischemia and reperfusion. Chlorpromazine and trifluoperazine, calmodulin inhibitors, were used to enhance myocardial preservation by preventing harmful effect of intracellular calcium

(N-3) long-chain polyunsaturated fatty acids prolong survival following myocardial infarction in rats.

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Many clinical studies report that (n-3) PUFAs decrease the incidence of sudden death in patients with coronary artery disease after myocardial infarction (MI). However, the mechanisms for the beneficial effects of (n-3) PUFAs are unknown. The objectives of the present study were to confirm the

Genetic susceptibility for ischemic infarction and arteriolosclerosis based on neuropathologic evaluations.

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BACKGROUND Recent genetic studies of stroke and related risk factors have identified a growing number of susceptibility loci; however, the relationship of these alleles to ischemic stroke is unknown. The challenge in finding reproducible loci of ischemic stroke susceptibility may be in part related

Intracerebroventricular administration of morphine confers remote cardioprotection--role of opioid receptors and calmodulin.

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The current study aimed to delineate the mechanism of remote preconditioning by intracerebroventricular morphine (RMPC) against myocardial ischemia-reperfusion injury. Male Sprague-Dawley rats were given an intracerebroventricular morphine injection before myocardial ischemia and reperfusion injury.

Selective modulation of coupled ryanodine receptors during microdomain activation of calcium/calmodulin-dependent kinase II in the dyadic cleft.

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BACKGROUND In ventricular myocytes of large mammals with low T-tubule density, a significant number of ryanodine receptors (RyRs) are not coupled to the sarcolemma; cardiac remodeling increases noncoupled RyRs. OBJECTIVE Our aim was to test the hypothesis that coupled and noncoupled RyRs have

Moderation of myocardial ischemia reperfusion injury by calcium channel and calmodulin receptor inhibition.

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Intracellular Ca2+ accumulation is implicated in the pathogenesis of myocardial reperfusion injury. To study approaches designed to modify Ca2+ uptake during coronary revascularization after acute infarction, a pig heart surgical infarct model (left anterior descending artery occlusion for 60 min)

Alteration of protein expression profile following voluntary exercise in the perilesional cortex of rats with focal cerebral infarction.

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Identification of functional molecules in the brain related to improvement of the degree of paralysis or increase of activities will contribute to establishing a new treatment strategy for stroke rehabilitation. Hence, protein expression changes in the cerebral cortex of rat groups with/without

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