Dynamics of Ca2+/calmodulin-dependent protein kinase II following acute myocardial ischemia—translocation and autophosphorylation

Uemura, Arata; Naito, Yasuhito

doi:10.1016/s0006-291x(02)02279-9

Cited by 15 publications

(14 citation statements)

References 29 publications

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“…These observations indirectly suggest that CaMKII may be an important mediator in the cardioprotection of IHA hypoxia. In the present study, we confirm that I/R decreases SR and cytosolic CaMKII activity, a consistent result with the observation from similar I/R model (30,37). Interestingly, IHA hypoxia significantly preserves SR CaMKII activity during reperfusion, but it does not affect CaMKII protein abundance and cytosolic CaMKII activity.…”

Section: Discussionsupporting

confidence: 93%

Calcium/calmodulin-dependent protein kinase II mediates cardioprotection of intermittent hypoxia against ischemic-reperfusion-induced cardiac dysfunction

Yu¹,

Wang²,

Yang³

2009

American Journal of Physiology-Heart and Circulatory Physiology

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Intermittent high-altitude (IHA) hypoxia-induced cardioprotection against ischemia-reperfusion (I/R) injury is associated with the preservation of sarcoplasmic reticulum (SR) function. Although Ca(2+)/calmodulin (CaM)-dependent protein kinase II (CaMKII) and phosphatase are known to modulate the function of cardiac SR under physiological conditions, the status of SR CaMKII and phosphatase during I/R in the hearts from IHA hypoxic rats is unknown. In the present study, we determined SR and cytosolic CaMKII activity during preischemia and I/R (30 min/30 min) in perfused hearts from normoxic and IHA hypoxic rats. The left ventricular contractile recovery, SR CaMKII activity as well as phosphorylation of phospholamban at Thr(17), and Ca(2+)/CaM-dependent SR Ca(2+)-uptake activity were depressed in the I/R hearts from normoxic rats, whereas these changes were prevented in the hearts from IHA hypoxic rats. Such beneficial effects of IHA hypoxia were lost by treating the hearts with a specific CaMKII inhibitor, KN-93. I/R also depressed cytosolic CaMKII and SR phosphatase activity, but these alterations remained unchanged in IHA hypoxic group. Furthermore, we found that the autophosphorylation at Thr(287), which confers Ca(2+)/CaM-independent activity, was not altered by I/R in both groups. These findings indicate that preservation of SR CaMKII activity plays an important role in the IHA hypoxia-induced cardioprotection against I/R injury via maintaining SR Ca(2+)-uptake activity.

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Section: Discussionsupporting

confidence: 93%

Calcium/calmodulin-dependent protein kinase II mediates cardioprotection of intermittent hypoxia against ischemic-reperfusion-induced cardiac dysfunction

Yu¹,

Wang²,

Yang³

2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…The frozen hearts were weighed, minced and homogenized in 5 volume buffer (in mmol/l, TrisHCl [pH 7.5] 30, DTT 1, EDTA 1, EGTA 1, leupeptin 0.02, and phenylmethanesulfonyl fluoride 0.2). Homogenates were centrifuged at 1,000 × g for 15 min, and the supernatants were then centrifuged at 100,000 × g for 1 h at 4°C to separate the cytosolic fraction (12). Aliquots of protein from the cytosolic fractions were separated by SDS-PAGE, which was performed according to the method of Laemmli on 10% acrylamide gels (13), and transferred electrophoretically onto Immobilon P (Millipore) membranes.…”

Section: Western Blot Analysismentioning

confidence: 99%

“…The main purpose of the present study was to perform a noninvasive evaluation of the time course of changes in car- 4,6,8,12,16,20 …”

Section: Introductionmentioning

confidence: 99%

Noninvasive Evaluation of the Time Course of Change in Cardiac Function in Spontaneously Hypertensive Rats by Echocardiography

et al. 2005

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“…46 It has been demonstrated that I/R injury induces compartmentalization of CaMK II during transient ischemia with subsequent redistribution during reperfusion. 47 CaMK II translocation was not tested in our study. However, it is possible that CaMK II translocation might play a role in desflurane-induced postconditioning.…”

Section: Discussionmentioning

confidence: 97%

Desflurane-induced Postconditioning Is Mediated by β-Adrenergic Signaling

Lange¹,

Redel²,

Lotz³

et al. 2009

Anesthesiology

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Background: Anesthetic preconditioning is mediated by ␤-adrenergic signaling. This study was designed to elucidate the role of ␤-adrenergic signaling in desflurane-induced postconditioning.Methods: Pentobarbital-anesthetized New Zealand White rabbits were subjected to 30 min of coronary artery occlusion followed by 3 h of reperfusion and were randomly assigned to receive vehicle (control), 1.0 minimum alveolar concentration of desflurane, esmolol (30 mg ⅐ kg ؊1 ⅐ h ؊1 ) for the initial 30 min

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Dynamics of Ca2+/calmodulin-dependent protein kinase II following acute myocardial ischemia—translocation and autophosphorylation

Cited by 15 publications

References 29 publications

Calcium/calmodulin-dependent protein kinase II mediates cardioprotection of intermittent hypoxia against ischemic-reperfusion-induced cardiac dysfunction

Calcium/calmodulin-dependent protein kinase II mediates cardioprotection of intermittent hypoxia against ischemic-reperfusion-induced cardiac dysfunction

Noninvasive Evaluation of the Time Course of Change in Cardiac Function in Spontaneously Hypertensive Rats by Echocardiography

Desflurane-induced Postconditioning Is Mediated by β-Adrenergic Signaling

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