Cited by 367Cardiac Ischemia and ReperfusionNitric Oxide and Endothelin EffectsRedox biology and oxidative stress

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Preconditioning Results in S -Nitrosylation of Proteins Involved in Regulation of Mitochondrial Energetics and Calcium Transport

Sun, Junhui, Morgan, Meghan, Shen, Rong-Fong, Steenbergen, Charles, Murphy, Elizabeth·2007·Circulation Research

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Abstract

Nitric oxide has been shown to be an important signaling messenger in ischemic preconditioning (IPC). Accordingly, we investigated whether protein S -nitrosylation occurs in IPC hearts and whether S -nitrosoglutathione (GSNO) elicits similar effects on S -nitrosylation and cardioprotection. Preceding 20 minutes of no-flow ischemia and reperfusion, hearts from C57BL/6J mice were perfused in the Langendorff mode and subjected to the following conditions: (1) control perfusion; (2) IPC; or (3) 0.1 mmol/L GSNO treatment. Compared with control, IPC and GSNO significantly improved postischemic recovery of left ventricular developed pressure and reduced infarct size. IPC and GSNO both significantly increased S -nitrosothiol contents and S -nitrosylation levels of the L-type Ca 2+ channel α1 subunit in heart membrane fractions. We identified several candidate S -nitrosylated proteins by proteomic analysis following the biotin switch method, including the cardiac sarcoplasmic reticulum Ca 2+ -ATPase, α-ketoglutarate dehydrogenase, and the mitochondrial F1-ATPase α1 subunit. The activities of these enzymes were altered in a concentration-dependent manner by GSNO treatment. We further developed a 2D DyLight fluorescence difference gel electrophoresis proteomic method that used DyLight fluors and a modified biotin switch method to identify S -nitrosylated proteins. IPC and GSNO produced a similar pattern of S -nitrosylation modification and cardiac protection against ischemia/reperfusion injury, suggesting that protein S -nitrosylation may play an important cardioprotective role in heart.

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Authors: Sun, J., Morgan, M., Shen, R.-F., Steenbergen, C., & Murphy, E.
Affiliations: National Institutes of Health (US)
From the Vascular Medicine Branch (J.S., E.M.) and Proteomics Core Facility (M.M., R.-F.S.), National Heart Lung and Blood Institute, NIH, Bethesda; and Department of Pathology (C.S.), Johns Hopkins University, Baltimore, Md.
ORCID: Sun, Junhui
Shen, Rong-Fong
Steenbergen, Charles
Murphy, Elizabeth
Venue: Circulation Research
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2007-11-26
Volume: 101
Issue: 11
Pages: 1155-1163
ISSN: 0009-7330 (ISSN-L)
1524-4571
DOI: 10.1161/circresaha.107.155879
OpenAlex: W2126788226
Cited by: 367
References: 45
Citations by year: 2026: 4 · 2025: 13 · 2024: 11 · 2023: 11 · 2022: 3 · 2021: 14 · 2020: 12 · 2019: 18 · 2018: 16 · 2017: 20 · 2016: 15 · 2015: 20 · 2014: 35 · 2013: 34 · 2012: 32
FWCI: 16.99
Type: journal article
Language: en
Open access: closed
Locations: Circulation Research (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health
National Heart, Lung, and Blood Institute (R01HL039752, HL 39752)
National Institute of Environmental Health Sciences
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Keywords: ischemic preconditioning, S-nitrosylation, S-nitrosoglutathione, nitric oxide signaling, cardioprotection, myocardial ischemia-reperfusion injury, sarcoplasmic reticulum Ca2+-ATPase, alpha-ketoglutarate dehydrogenase, mitochondrial F1-ATPase, mitochondrial bioenergetics, calcium transport
MeSH terms: Animals, Biological Transport, Calcium, Cardiotonic Agents, Energy Metabolism, Mice, Inbred C57BL, Mitochondria, Nitrogen Oxides, Perfusion, Proteins, Myocardial Reperfusion Injury, Ventricular Dysfunction, Left, Ischemic Preconditioning, Myocardial, Mice, In Vitro Techniques

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Preconditioning Results in S -Nitrosylation of Proteins Involved in Regulation of Mitochondrial Energetics and Calcium Transport

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