Essential role of nitric oxide in acute ischemic preconditioning: S-Nitros(yl)ation versus sGC/cGMP/PKG signaling?

Sun, Junhui; Aponte, Angel; Kohr, Mark J.; Tong, Guang; Steenbergen, Charles; Murphy, Elizabeth

doi:10.1016/j.freeradbiomed.2012.09.005

Cited by 62 publications

(56 citation statements)

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“…217 In fact, NO directly targets several proteins and alters their structure and function through nitrosation or nitrosylation. 215,216 The nitrosylation is thought to shield cysteine residues from oxidation. 388 IPC, 215 POC, 389,390 and RIC 64 reduce IS independently from PKG, and several nitrosylated proteins were identified in preconditioned myocardium, notably also mitochondrial proteins.…”

Section: Hexokinasementioning

confidence: 99%

“…215,216 The nitrosylation is thought to shield cysteine residues from oxidation. 388 IPC, 215 POC, 389,390 and RIC 64 reduce IS independently from PKG, and several nitrosylated proteins were identified in preconditioned myocardium, notably also mitochondrial proteins. 215,388 Mitochondrial Cx 43 is a target of nitrosation during IPC.…”

Section: Hexokinasementioning

confidence: 99%

“…211,213 During POC, the sodium-proton exchanger is another target of PKG, and PKG activation delays the normalization of acidosis. 214 NO signals protection by IPC not only through PKG, but also through nitrosylation, 215,216 and the PKG-independent action of NO seems to occur at reperfusion.…”

mentioning

confidence: 99%

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Molecular Basis of Cardioprotection

Heusch

2015

Circulation Research

713

409

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Abstract:Reperfusion is mandatory to salvage ischemic myocardium from infarction, but reperfusion per se contributes to injury and ultimate infarct size. Therefore, cardioprotection beyond that by timely reperfusion is needed to reduce infarct size and improve the prognosis of patients with acute myocardial infarction. The conditioning phenomena provide such cardioprotection, insofar as brief episodes of coronary occlusion/ reperfusion preceding (ischemic preconditioning) or following (ischemic postconditioning) sustained myocardial ischemia with reperfusion reduce infarct size. Even ischemia/reperfusion in organs remote from the heart provides cardioprotection (remote ischemic conditioning). The present review characterizes the signal transduction underlying the conditioning phenomena, including their physical and chemical triggers, intracellular signal transduction, and effector mechanisms, notably in the mitochondria. Cardioprotective signal transduction appears as a highly concerted spatiotemporal program. Although the translation of ischemic postconditioning and remote ischemic conditioning protocols to patients with acute myocardial infarction has been fairly successful, the pharmacological recruitment of cardioprotective signaling has been largely disappointing to date.

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Section: Hexokinasementioning

confidence: 99%

Section: Hexokinasementioning

confidence: 99%

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Molecular Basis of Cardioprotection

Heusch

2015

Circulation Research

713

409

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“…Moreover, a PubMed search for the words "S-nitrosylation and cardioprotection" gives out sixteen 154 , the authors wonder whether or not "nitric oxide signaling differ in pre-and post-conditioning" and in particular they wonder whether "Snitrosylation is involved in postconditioning's protection". Below we will see that S-nitrosylation is involved in both ischemic and pharmacological postconditioning.…”

Section: Preconditioning and Postconditioningmentioning

confidence: 99%

Protein S-nitrosylation in preconditioning and postconditioning

Penna

Angotti

Pagliaro

2014

Exp Biol Med (Maywood)

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The coronary artery disease is a leading cause of death and morbidity worldwide. This disease has a complex pathophysiology that includes multiple mechanisms. Among these is the oxidative/nitrosative stress. Paradoxically, oxidative/nitrosative signaling plays a major role in cardioprotection against ischemia/reperfusion injury. In this context, the gas transmitter nitric oxide (NOֹ) may act through several mechanisms, such as guanylil cyclase activation and via Snitrosylation (SNO) of proteins. The latter is a covalent modification of a protein cysteine thiol by an NO-group that generates an S-nitrosothiol. Here we report data showing that NOֹ and SNO of proteins play a pivotal role not only in preconditioning, but also in postconditioning cardioprotection.

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“…Furthermore, NO regulates calcium homeostasis within the cell by enhancing calcium uptake into the sarcoplasmic reticulum [39], directly inhibits Ca 2+ influx across L-type calcium channels of the cardiomyocytes [40], modifies noradrenaline release from nerve endings [41], regulates free radical formation and protects the myocardium against reperfusion injury [42,43]. Some of these effects are not mediated by cGMP; there is increasing evidence that NO may modify processes and functions by a cGMPindependent way, with S-nitrosylation [44]. Nevertheless, all these above mentioned effects and mechanisms of NO may somehow contribute to the antiarrhythmic effect of preconditioning.…”

Section: Sudden Cardiac Death and Preconditioningmentioning

confidence: 99%

The effect of acute simvastatin administration on the ischaemia and reperfusion-induced ventricular arrhythmias in anesthetized dogs

Kisvári¹

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SUMMARYVentricular tachyarrhythmia is one of the main causes responsible for sudden cardiac death. The prevention and treatment of these severe tachyarrhythmias is still remained a big challenge of cardiology in the industrialized countries. There is increasing evidence that statins, which represent the first-line therapy for hyperlipidaemia, may possess lipidindependent pleiotropic actions, which are associated with an increased release of nitric oxide (NO) through the activation of eNOS, and contribute to cardioprotection following chronic statin treatment. There is lack of evidence, however, whether statins administered acutely influence the severity of arrhythmias, resulting from ischaemia and reperfusion (I/R).Therefore, the aim of the present study was to examine the effects and mechanisms of acute statin administration on arrhythmias resulting from a 25 min coronary artery occlusion and reperfusion (I/R) in chloralose/urethane anaesthetized dogs. In a group of dogs activated simvastatin (0.1 mg/kg) was administrated in slow intracoronary injection just prior to the occlusion of the left anterior descending coronary artery. The severity of ischaemia (degree of inhomogeneity of electrical activation, epicardial ST-segment) and of arrhythmias, as well as the plasma NOx levels in blood samples taken from the coronary sinus were assessed. From the myocardial tissue samples the activity of eNOS (Western blot) and superoxide production (confocal microscopy) were determined.We have shown that compared to the control group, in which the dogs were treated only with the solvent of simvastatin, the administration of simvastatin significantly decreased the severity of ischaemia and of ventricular arrhythmias, increased the activity of eNOS and the plasma concentration of NO metabolites, and significantly reduced the production of superoxide during reperfusion. We have also pointed out that the protective effects of simvastatin are mediated through the rapid activation of eNOS, most probably via the stimulation of PI-3 kinase/Akt pathway, since the inhibition of NOS by L-NAME, and the inhibition PI-3 kinase by wortmannin abolished the protective effects of simvastatin.Thus we conclude that the antiarrhythmic effect of acute simvastatin administration can certainly be associated with an increased NO bioavailability during occlusion, due to the rapid activation of eNOS via the stimulation of the PI3/Akt pathway by simvastatin.

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Essential role of nitric oxide in acute ischemic preconditioning: S-Nitros(yl)ation versus sGC/cGMP/PKG signaling?

Cited by 62 publications

References 50 publications

Molecular Basis of Cardioprotection

Molecular Basis of Cardioprotection

Protein S-nitrosylation in preconditioning and postconditioning

The effect of acute simvastatin administration on the ischaemia and reperfusion-induced ventricular arrhythmias in anesthetized dogs

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