Cardioprotective effect with carbon monoxide releasing molecule-2 (CORM-2) in isolated perfused rat heart: Role of coronary endothelium and underlying mechanism

Soni, Hitesh; Patel, Praful; Rath, Akshyaya; Jain, Mukul; Mehta, Abhishek

doi:10.1016/j.vph.2010.04.002

Cited by 34 publications

(28 citation statements)

References 49 publications

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“…Moreover, CORM-2 showed significantly improved post-ischaemic recovery of heart rate, coronary flow rate, cardiodynamic parameters and reduced infarct size (Soni et al, 2012). PC with CORM-2 in rat isolated hearts markedly decreased LDH and CK levels in coronary effluent after global ischaemia, providing also a significant improvement in coronary flow rate, heart rate, cardiodynamic parameters and marked attenuation in infarct size (Soni et al, 2010). In addition, marked LV dysfunction following coronary artery occlusion and reperfusion was ameliorated by CORM-3 in mouse hearts (Clark et al, 2009).…”

Section: Experimental Model Effect Of H2s Proposed Mechanism(s) Refermentioning

confidence: 91%

“…The mechanism by which CORM-2 triggers PC in rat isolated hearts is probably due to the activation of the p38 MAPK β and PKC pathways before ischaemia as well as PI3-kinase pathway during reperfusion (Soni et al, 2012) and activation of the K ATP channels (Soni et al, 2010).…”

Section: Experimental Model Effect Of H2s Proposed Mechanism(s) Refermentioning

confidence: 99%

“…Cardiomyocytes ( Rat isolated hearts (CO exposure) Increased the baseline coronary flow and the contracture magnitude, improved contractile recovery and ventricular arrhythmia incidence, and increased the hyperemic coronary flow CO-exposed hearts could be preconditioned in the same way as normal myocardium Rochetaing et al (2001) Rat isolated hearts (PC with CORM-2) Reduction of infarct size Activation of the p38 MAPK β and PKC pathways before ischaemia and of PI3-kinase pathway during reperfusion Soni et al (2012) Rat isolated hearts (PC with CORM-2) Marked attenuation of infarct size Activation of the KATP channels Soni et al (2010) Mouse hearts (CORM-3) Amelioration of LV dysfunction Clark et al (2009) Isolated hearts (CORM-3) Reduction in cardiac muscle damage and infarct size Activation of mitoKATP channels Clark et al (2003) Isolated hearts (CORM-2) Reduction of infarct size Activation of mitoKATP channels -NOS-cGMP and HO-1 pathways Mei et al (2007) In vivo (mice) CORM-3 (24 h prior to coronary occlusion)…”

Section: Experimental Model Effect Of Co Proposed Mechanism(s) Referencementioning

confidence: 99%

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The role of gasotransmitters NO, H₂S and CO in myocardial ischaemia/reperfusion injury and cardioprotection by preconditioning, postconditioning and remote conditioning

Andreadou

Iliodromitis

Rassaf

et al. 2014

British J Pharmacology

173

150

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Ischaemic heart disease is one of the leading causes of morbidity and mortality worldwide. The development of cardioprotective therapeutic agents remains a partly unmet need and a challenge for both medicine and industry, with significant financial and social implications. Protection of the myocardium can be achieved by mechanical vascular occlusions such as preconditioning (PC), when brief episodes of ischaemia/reperfusion (I/R) are experienced prior to ischaemia; postconditioning (PostC), when the brief episodes are experienced at the immediate onset of reperfusion; and remote conditioning (RC), when the brief episodes are experienced in another vascular territory. The elucidation of the signalling pathways, which underlie the protective effects of PC, PostC and RC, would be expected to reveal novel molecular targets for cardioprotection that could be modulated by pharmacological agents to prevent reperfusion injury. Gasotransmitters including NO, hydrogen sulphide (H2S) and carbon monoxide (CO) are a growing family of regulatory molecules that affect physiological and pathological functions. NO, H2S and CO share several common properties; they are beneficial at low concentrations but hazardous in higher amounts; they relax smooth muscle cells, inhibit apoptosis and exert anti-inflammatory effects. In the cardiovascular system, NO, H2S and CO induce vasorelaxation and promote cardioprotection. In this review article, we summarize current knowledge on the role of the gasotransmitters NO, H2S and CO in myocardial I/R injury and cardioprotection provided by conditioning strategies and highlight future perspectives in cardioprotection by NO, H2S, CO, as well as their donor molecules. LINKED ARTICLESThis article is part of a themed section on Pharmacology of the Gasotransmitters. To view the other articles in this section visit http://dx. Abbreviations 3MP, 3-mercaptopyruvate; 3-MST, 3-mercaptopyruvate transferase; BCA, cyano-L-alanine; CBS, cystathionine β-synthase; CHD, coronary heart disease; CK, creatinine kinase; CORM, carbon monoxide-releasing molecule; CSE, cystathionine γ-lyase; CyPD, cyclophilin D; HPDTT, 5-(4-hydroxyphenyl)-3H-1,2-dithiole-3-thione; eNOS, endothelial nitric oxide synthase; FeTPPS, 5,10,15, porphyrinato iron; GYY4137, morpholin-4-ium 4-methoxyphenyl-morpholino-phosphinodithioate; HNO, nitroxyl; HO, haem oxygenase; I/R, ischaemia/reperfusion; iNOS, inducible nitric oxide synthase; L-NAME, N-nitro-L-arginine methylester; L-NNA, Nω-nitro-l-arginine; LV, left ventricular; MitoSNO, mitochondria-targeted S-nitrosothiols; mPTP, mitochondria permeability transition pore; nNOS, neuronal nitric oxide synthase; Nrf2, nuclear factor (erythroid-derived 2)-like 2; NSAIDs, non-steroidal antiinflammatory drugs; ONOO − , peroxynitrite; PRG, DL-propargylglycine; PC, preconditioning; PostC, postconditioning; RC, remote conditioning; RISK, reperfusion injury salvage kinase; ROS, reactive oxygen species; SAC, S-allylcysteine; SAFE, survivor activating factor enhancement; SOD, superoxide dismutase; XOR, xanthin...

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Section: Experimental Model Effect Of H2s Proposed Mechanism(s) Refermentioning

confidence: 91%

Section: Experimental Model Effect Of H2s Proposed Mechanism(s) Refermentioning

confidence: 99%

Section: Experimental Model Effect Of Co Proposed Mechanism(s) Referencementioning

confidence: 99%

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The role of gasotransmitters NO, H₂S and CO in myocardial ischaemia/reperfusion injury and cardioprotection by preconditioning, postconditioning and remote conditioning

Andreadou

Iliodromitis

Rassaf

et al. 2014

British J Pharmacology

173

150

View full text Add to dashboard Cite

show abstract

“…CO (or CORM) also modulates non-cardiac ion channels, with potential repercussions on cardiovascular function. For example, the activation of the I KATP channel in vascular smooth muscle cells may account for the cardioprotective effect of CORM-2 observed in the perfused rat heart (Soni et al, 2010) since this effect is reversed by glibenclamide. CO also activates TREK-1 (tandem pore-domain K + channel), and inhibits native or recombinant Kv 2.1 (Dallas et al, 2011), which may be cardiprotective (Dhalla et al, 2000;Honore, 2007).…”

Section: Beneficial Effects Of Comentioning

confidence: 99%

Carbon monoxide exposure in the urban environment: An insidious foe for the heart?

Reboul

Thireau

Meyer

et al. 2012

Respiratory Physiology & Neurobiology

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“…In mammalian cells CO is generated by the enzyme heme-oxygenase [4]. CO participates in the regulation of a wide variety of cellular functions [5,6,7,8,9] and contributes to the regulation of cell death [10,11,12,13,14,15]. CO may elicit both vasodilation and vasoconstriction [16,17].…”

Section: Introductionmentioning

confidence: 99%

Effect of Carbon Monoxide Donor CORM-2 on Vitamin D<sub>3</sub> Metabolism

Feger

Fajol

Lebedeva

et al. 2013

Kidney Blood Press Res

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Background/Aims: Carbon monoxide (CO) interferes with cytochrome-dependent cellular functions and acts as gaseous transmitter. CO is released from CO-releasing molecules (CORM) including tricarbonyl-dichlororuthenium (II) dimer (CORM-2), molecules considered for the treatment of several disorders including vascular dysfunction, inflammation, tissue ischemia and organ rejection. Cytochrome P450-sensitive function include formation of 1,25-dihydroxyvitamin D₃ (1,25(OH)₂D₃) by renal 25-hydroxyvitamin D₃ 1-alpha-hydroxylase (Cyp27b1). The enzyme is regulated by PTH, FGF23 and klotho. 1,25(OH)₂D₃ regulates Ca²⁺ and phosphate transport as well as klotho expression. The present study explored, whether CORM-2 influences 1,25(OH)₂D₃ formation and klotho expression. Methods: Mice were treated with intravenous CORM-2 (20 mg/kg body weight). Plasma 1,25(OH)₂D₃ and FGF23 concentrations were determined by ELISA, phosphate, calcium and creatinine concentrations by colorimetric methods, transcript levels by quantitative RT-PCR and protein expression by western blotting. Fgf23 mRNA transcript levels were further determined in rat osteosarcoma UMR106 cells without or with prior treatment for 24 hours with 20 µM CORM-2. Results: CORM-2 injection within 24 hours significantly increased FGF23 plasma levels and decreased 1,25(OH)₂D₃ plasma levels, renal Cyp27b1 gene expression as well as renal klotho protein abundance and transcript levels. Moreover, treatment of UMR106 cells with CORM-2 significantly increased Fgf23 transcript levels. Conclusion: CO-releasing molecule CORM-2 enhances FGF23 expression and release and decreases klotho expression and 1,25(OH)₂D₃ synthesis.

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Cardioprotective effect with carbon monoxide releasing molecule-2 (CORM-2) in isolated perfused rat heart: Role of coronary endothelium and underlying mechanism

Cited by 34 publications

References 49 publications

The role of gasotransmitters NO, H₂S and CO in myocardial ischaemia/reperfusion injury and cardioprotection by preconditioning, postconditioning and remote conditioning

The role of gasotransmitters NO, H₂S and CO in myocardial ischaemia/reperfusion injury and cardioprotection by preconditioning, postconditioning and remote conditioning

Carbon monoxide exposure in the urban environment: An insidious foe for the heart?

Effect of Carbon Monoxide Donor CORM-2 on Vitamin D<sub>3</sub> Metabolism

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Cardioprotective effect with carbon monoxide releasing molecule-2 (CORM-2) in isolated perfused rat heart: Role of coronary endothelium and underlying mechanism

Cited by 34 publications

References 49 publications

The role of gasotransmitters NO, H2S and CO in myocardial ischaemia/reperfusion injury and cardioprotection by preconditioning, postconditioning and remote conditioning

The role of gasotransmitters NO, H2S and CO in myocardial ischaemia/reperfusion injury and cardioprotection by preconditioning, postconditioning and remote conditioning

Carbon monoxide exposure in the urban environment: An insidious foe for the heart?

Effect of Carbon Monoxide Donor CORM-2 on Vitamin D<sub>3</sub> Metabolism

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Product

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The role of gasotransmitters NO, H₂S and CO in myocardial ischaemia/reperfusion injury and cardioprotection by preconditioning, postconditioning and remote conditioning

The role of gasotransmitters NO, H₂S and CO in myocardial ischaemia/reperfusion injury and cardioprotection by preconditioning, postconditioning and remote conditioning