Protein S-nitrosylation in preconditioning and postconditioning

Penna, Cláudia; Angotti, Carmelina; Pagliaro, Pasquale

doi:10.1177/1535370214522935

Cited by 35 publications

(54 citation statements)

References 212 publications

(511 reference statements)

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“…Before considering the sources of ROS/RNS, here we briefly review the biochemistry and biology of the reactive species. Although reactions to RNS will be considered in more detail, the reader is kindly redirected to more focused reviews on this topic (Espey et al ., ; Becker, ; Martínez and Andriantsitohaina, ; Heinrich et al ., ; Penna et al ., ).…”

Section: Ros/rns and Oxidative/nitrosative Signalling Or Stressmentioning

confidence: 97%

“…The non‐NOS process of ● NO formation includes non‐enzymatic reactions that are favoured by acidic conditions, such as the reduction of nitrite to ● NO, and reactions catalysed by non‐NOS enzymes, such as cytochrome c , Hb and xanthine oxidoreductase (Zweier et al ., ). Molecular targets of ● NO include metalloenzymes (especially sGC, Hb and cytochromes) and thiols yielding S ‐nitrosothiols (see also below) (Ferdinandy and Schulz, ; Pacher et al ., ; Penna et al ., ). The major biological reaction of ● NO includes oxidation to nitrite and nitrate.…”

Section: Ros/rns and Oxidative/nitrosative Signalling Or Stressmentioning

confidence: 97%

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Redox signalling and cardioprotection: translatability and mechanism

Pagliaro

Penna

2015

British J Pharmacology

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The morbidity and mortality from coronary artery disease (CAD) remain significant worldwide. The treatment for acute myocardial infarction has improved over the past decades, including early reperfusion of culprit coronary arteries. Although it is mandatory to reperfuse the ischaemic territory as soon as possible, paradoxically this leads to additional myocardial injury, namely ischaemia/reperfusion (I/R) injury, in which redox stress plays a pivotal role and for which no effective therapy is currently available. In this review, we report evidence that the redox environment plays a pivotal role not only in I/R injury but also in cardioprotection. In fact, cardioprotective strategies, such as pre-and post-conditioning, result in a robust reduction in infarct size in animals and the role of redox signalling is of paramount importance in these conditioning strategies. Nitrosative signalling and cysteine redox modifications, such as S-nitrosation/S-nitrosylation, are also emerging as very important mechanisms in conditioning cardioprotection. The reasons for the switch from protective oxidative/nitrosative signalling to deleterious oxidative/nitrosative/nitrative stress are not fully understood. The complex regulation of this switch is, at least in part, responsible for the diminished or lack of cardioprotection induced by conditioning protocols observed in ageing animals and with co-morbidities as well as in humans. Therefore, it is important to understand at a mechanistic level the reasons for these differences before proposing a safe and useful transition of ischaemic or pharmacological conditioning. Indeed, more mechanistic novel therapeutic strategies are required to protect the heart from I/R injury and to improve clinical outcomes in patients with CAD. LINKED ARTICLESThis article is part of a themed section on Conditioning the Heart -Pathways to Translation. To view the other articles in this section visit http://dx.doi. org/10.1111/bph.2015.172.issue-8 Abbreviations AMI, acute myocardial infarction; CVD, cardiovascular disease; I/R, ischaemia/reperfusion; I-PostC, ischaemic post-conditioning; I-PreC, ischaemic preconditioning; mitoKATP, mitochondrial ATP-activated K + channel; MPG, mercaptopropionyl glycine; mPTP, mitochondrial permeability transition pore; NAC, N-acetylcysteine; ODQ, 1H- [1,2,4]oxadiazole [4,3,-α]quinoxaline-1-one; RIRR, ROS-induced ROS release; RISK, reperfusion injury salvage kinase; RNS, reactive nitrogen species; ROS, reactive oxygen species; SAFE, survivor activating factor enhancement; SERCA, sarco/endoplasmatic reticulum calcium ATPase; SOD, superoxide dismutase; STEMI, ST-segment elevation myocardial infarction; XOR, xanthine oxo-reductase BJP IntroductionThe prevalence of chronic and degenerative diseases, including cardiovascular disease (CVD), is increasing worldwide. Acute coronary syndromes, including myocardial infarction, are the most typical examples of pathologies with a strong redox-sensitive component and remain the leading cause of death in Western countries despite ...

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Section: Ros/rns and Oxidative/nitrosative Signalling Or Stressmentioning

confidence: 97%

Section: Ros/rns and Oxidative/nitrosative Signalling Or Stressmentioning

confidence: 97%

Redox signalling and cardioprotection: translatability and mechanism

Pagliaro

Penna

2015

British J Pharmacology

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“…Of note, this posttranslational modification of a L-type calcium channel subunit has already been described in preconditioning cardioprotection by Murphy et al (2014) and in non-ischemic hearts treated with CST by Angelone et al (2012b). The CST-Post-elicited S-nitrosylation of calcium channel may be functionally important, since the oxidative/nitrosative signaling is known to play a major role in cardioprotection against ischemia/reperfusion injury in both preconditioning and post-conditioning (Pagliaro et al, 2011; Tullio et al, 2013; Penna et al, 2014b). …”

Section: Cardioprotective Influence Of Vs-1 and Cstmentioning

confidence: 99%

The surging role of Chromogranin A in cardiovascular homeostasis

2014

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Together with Chromogranin B and Secretogranins, Chromogranin A (CGA) is stored in secretory (chromaffin) granules of the diffuse neuroendocrine system and released with noradrenalin and adrenalin. Co-stored within the granule together with neuropeptideY, cardiac natriuretic peptide hormones, several prohormones and their proteolytic enzymes, CGA is a multifunctional protein and a major marker of the sympatho-adrenal neuroendocrine activity. Due to its partial processing to several biologically active peptides, CGA appears an important pro-hormone implicated in relevant modulatory actions on endocrine, cardiovascular, metabolic, and immune systems through both direct and indirect sympatho-adrenergic interactions. As a part of this scenario, we here illustrate the emerging role exerted by the full-length CGA and its three derived fragments, i.e., Vasostatin 1, catestatin and serpinin, in the control of circulatory homeostasis with particular emphasis on their cardio-vascular actions under both physiological and physio-pathological conditions. The Vasostatin 1- and catestatin-induced cardiodepressive influences are achieved through anti-beta-adrenergic-NO-cGMP signaling, while serpinin acts like beta1-adrenergic agonist through AD-cAMP-independent NO signaling. On the whole, these actions contribute to widen our knowledge regarding the sympatho-chromaffin control of the cardiovascular system and its highly integrated “whip-brake” networks.

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“…Perspective directions of investigations in 41 the field include development of sophisticated classification of oxidative stresses, accurate identification 42 of cellular ROS targets and their arranged responses to ROS influence, real in situ functions and operation 43 of so-called ''antioxidants'', intracellular spatiotemporal distribution and effects of ROS, deciphering of 44 molecular mechanisms responsible for cellular response to ROS attacks, and ROS involvement in realiza- 45 tion of normal cellular functions in cellular homeostasis. 46 Ó 2014 Elsevier Ireland Ltd. All rights reserved. 47 1.…”

mentioning

confidence: 95%

“…219 Glutathione level is finely adjusted by organisms to specific condi-220 tions via several regulatory pathways. Interestingly, GSH as other 221 thiols may interact with nitric oxide ( Å NO) to neutralize it and at 222 the same time providing additional regulatory mechanism for 223 ROS-related processes like s-nitrosylation [43][44][45][46][47][48] …”

mentioning

confidence: 99%