WITHDRAWN: Infarct size limitation by adrenomedullin: Protein kinase A but not PI3-kinase is linked to mitochondrial KCa channels

Nishida, Hitoshi; Sato, Toshiaki; Miyazaki, Masaru; Nakaya, Haruaki

doi:10.1016/j.cardiores.2007.07.015

Cited by 28 publications

(35 citation statements)

References 53 publications

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“…However, at present, the signal transduction pathway(s) linking adenosine A 1 receptor activation with BK Ca channel opening are not known. Previous studies have shown that BK Ca channel activation via the k-opioid receptor and adrenomedullin involve PKC and PKA, respectively (Cao et al 2005a;Nishida et al 2008). It will be interesting to establish whether any of the protein kinases (PKC, ERK1/ 2, and p38 MAPK) associated with the cardioprotective effects of the adenosine A 1 receptor trigger BK Ca channel opening.…”

Section: Discussionmentioning

confidence: 99%

Role of large-conductance Ca²⁺-activated K⁺ channels in adenosine A₁ receptor-mediated pharmacological postconditioning in H9c2 cells

Fretwell

Dickenson

2011

Can. J. Physiol. Pharmacol.

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Ischaemic postconditioning is a phenomenon whereby short periods of ischaemia applied during the start of reperfusion protect the myocardium from the damaging consequences of reperfusion. As such, pharmacological-induced postconditioning represents an attractive therapeutic strategy for reducing reperfusion injury during cardiac surgery and following myocardial infarction. The primary aim of this study was to determine the role of large-conductance Ca 2+ -activated potassium channels (BKCa channels) in adenosine A1 receptor-induced pharmacological postconditioning in the rat embryonic cardiomyoblast-derived cell line H9c2. H9c2 cells were exposed to 6 h hypoxia (0.5% O2) followed by 18 h reoxygenation (H/R) after which cell viability was assessed by monitoring lactate dehydrogenase (LDH) release and caspase-3 activation. The adenosine A1 receptor agonist N 6 -cyclopentyladenosine (CPA; 100 nmol/L) or the BKCa channel opener NS1619 (10 mmol/L) were added for 30 min at the start of reoxygenation following 6 h hypoxic exposure. Where appropriate, cells were treated (15 min) before pharmacological postconditioning with the BKCa channel blockers paxilline (1 mmol/L) or iberiotoxin (100 nmol/L). Pharmacological postconditioning with CPA or NS1619 significantly reduced H/R-induced LDH release. Treatment with paxilline or iberiotoxin attenuated adenosine A1 receptor and NS1619-induced pharmacological postconditioning. These results have shown for the first time that BK Ca channels are involved in adenosine A 1 receptor-induced pharmacological postconditioning in a cell model system.Key words: adenosine, H9c2 cells, large-conductance Ca 2+ -activated potassium channel, hypoxia, adenosine A 1 receptor, pharmacological postconditioning. Résumé :Le postconditionnement ischémique est un phénomène par lequel de brèves périodes d'ischémie appliquées au début de la reperfusion protègent le myocarde contre les effets préjudiciables de la reperfusion. En tant que tel, le postconditionnement induit de manière pharmacologique représente une stratégie thérapeutique attrayante pour diminuer la lésion de reperfusion durant une intervention cardiaque et après un infarctus du myocarde. La présente étude a eu comme principal objectif de déterminer le rôle des canaux potassiques de grande conductance activés par le Ca 2+

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Section: Discussionmentioning

confidence: 99%

Role of large-conductance Ca²⁺-activated K⁺ channels in adenosine A₁ receptor-mediated pharmacological postconditioning in H9c2 cells

Fretwell

Dickenson

2011

Can. J. Physiol. Pharmacol.

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“…2, AM significantly increased the oxidative effect of NS1619 even in the presence of LY294002, a potent inhibitor of PI3-K. Moreover, erythropoietin, a potent activator of PI3-K (33, 34), did not augment the NS1619-induced flavoprotein oxidation (28). These results suggest that the mitoK Ca channel is not regulated by PI3-K. On the other hand, it is unclear whether activation of the PI3-K /Akt pathway modulates the opening of mitoK ATP channels.…”

Section: Mitochondrial Kmentioning

confidence: 90%

New Aspects for the Treatment of Cardiac Diseases Based on the Diversity of Functional Controls on Cardiac Muscles: Mitochondrial Ion Channels and Cardioprotection

et al. 2009

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Mitochondrial ATP-sensitive K + (mitoK ATP ) and Ca 2+ -activated K + (mitoK Ca ) channels exist in cardiac myocytes, and they play key roles in cardioprotection. We have recently reported that K + influx through mitoK ATP or mitoK Ca channels occurs independently of each other and confers cardioprotection in a similar manner. Activation of mitoK ATP channel is augmented by protein kinase C (PKC), whereas mitoK Ca channel is activated by protein kinase A (PKA). However, phosphatidylinositol 3-kinase (PI3-K) is linked to neither mitoK ATP nor mitoK Ca channels. We have demonstrated that bioactive substances modulate the opening of mitoK ATP channels via a PKC-dependent pathway or opening of mitoK Ca channels via a PKA-dependent pathway and thereby protecting the heart from ischemia/reperfusion injury. Several endogenous substances such as adenosine and bradykinin can reduce infarct size by activation of mitoK ATP channels in a PKC-dependent manner. Adrenomedullin, a potent vasodilator peptide, potentiates the opening of mitoK Ca channels by PKA activation. Treatment with adrenomedullin prior to ischemia results in the reduction of infarct size via a PKA-mediated activation of mitoK Ca channels. Thus, some endogenous substances confer cardioprotection via PKA-or PKC-mediated activation of mitoK ATP or mitoK Ca channels.

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“…Adult rabbit ventricular myocytes were isolated by collagenase digestion, as described previously (Nishida et al, 2008). Hearts were excised from anesthetized (i.v.…”

Section: Methodsmentioning

confidence: 99%

6-[4-(1-Cyclohexyl-1H-tetrazol-5-yl)butoxy]-3,4-dihydro-2-(1H)quinolinone (Cilostazol), a Phosphodiesterase Type 3 Inhibitor, Reduces Infarct Size via Activation of Mitochondrial Ca²⁺-Activated K⁺ Channels in Rabbit Hearts

Fukasawa¹,

Nishida²,

Sato³

et al. 2008

J Pharmacol Exp Ther

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WITHDRAWN: Infarct size limitation by adrenomedullin: Protein kinase A but not PI3-kinase is linked to mitochondrial KCa channels

Cited by 28 publications

References 53 publications

Role of large-conductance Ca²⁺-activated K⁺ channels in adenosine A₁ receptor-mediated pharmacological postconditioning in H9c2 cells

Role of large-conductance Ca²⁺-activated K⁺ channels in adenosine A₁ receptor-mediated pharmacological postconditioning in H9c2 cells

New Aspects for the Treatment of Cardiac Diseases Based on the Diversity of Functional Controls on Cardiac Muscles: Mitochondrial Ion Channels and Cardioprotection

6-[4-(1-Cyclohexyl-1H-tetrazol-5-yl)butoxy]-3,4-dihydro-2-(1H)quinolinone (Cilostazol), a Phosphodiesterase Type 3 Inhibitor, Reduces Infarct Size via Activation of Mitochondrial Ca²⁺-Activated K⁺ Channels in Rabbit Hearts

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WITHDRAWN: Infarct size limitation by adrenomedullin: Protein kinase A but not PI3-kinase is linked to mitochondrial KCa channels

Cited by 28 publications

References 53 publications

Role of large-conductance Ca2+-activated K+ channels in adenosine A1 receptor-mediated pharmacological postconditioning in H9c2 cells

Role of large-conductance Ca2+-activated K+ channels in adenosine A1 receptor-mediated pharmacological postconditioning in H9c2 cells

New Aspects for the Treatment of Cardiac Diseases Based on the Diversity of Functional Controls on Cardiac Muscles: Mitochondrial Ion Channels and Cardioprotection

6-[4-(1-Cyclohexyl-1H-tetrazol-5-yl)butoxy]-3,4-dihydro-2-(1H)quinolinone (Cilostazol), a Phosphodiesterase Type 3 Inhibitor, Reduces Infarct Size via Activation of Mitochondrial Ca2+-Activated K+ Channels in Rabbit Hearts

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Role of large-conductance Ca²⁺-activated K⁺ channels in adenosine A₁ receptor-mediated pharmacological postconditioning in H9c2 cells

Role of large-conductance Ca²⁺-activated K⁺ channels in adenosine A₁ receptor-mediated pharmacological postconditioning in H9c2 cells

6-[4-(1-Cyclohexyl-1H-tetrazol-5-yl)butoxy]-3,4-dihydro-2-(1H)quinolinone (Cilostazol), a Phosphodiesterase Type 3 Inhibitor, Reduces Infarct Size via Activation of Mitochondrial Ca²⁺-Activated K⁺ Channels in Rabbit Hearts