ArticleThe Journal of biological chemistry2010
Postischemic deactivation of cardiac aldose reductase: role of glutathione S-transferase P and glutaredoxin in regeneration of reduced thiols from sulfenic acids.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 53 citations in OpenAlex.
- Defining the S-Glutathionylation Proteome by Biochemical and Mass Spectrometric Approaches.Antioxidants (Basel, Switzerland) · 2022Review
- Glutathione in Protein Redox Modulation through S-Glutathionylation and S-Nitrosylation.Molecules (Basel, Switzerland) · 2021Review
- Cysteine modifications (oxPTM) and protein sulphenylation-mediated sulfenome expression in plants: evolutionary conserved signaling networks?Plant signaling & behavior · 2021Article
- Alcohol Binge Drinking Selectively Stimulates Protein S-Glutathionylation in Aorta and Liver ofFrontiers in cardiovascular medicine · 2021Article
- S-glutathionylation, friend or foe in cardiovascular health and disease.Redox biology · 2020Review
- Redox RegulationAntioxidants & redox signaling · 2020Review
- Sulodexide up-regulates glutathione S-transferase P1 by enhancing Nrf2 expression and translocation in human umbilical vein endothelial cells injured by oxygen glucose deprivation.Archives of medical science : AMS · 2020Article
- Acetaldehyde Induces an Endothelium-Dependent Relaxation of Superior Mesenteric Artery: Potential Role in Postprandial Hyperemia.Frontiers in physiology · 2019Article
- An evolving understanding of the S-glutathionylation cycle in pathways of redox regulation.Free radical biology & medicine · 2018Review
- ROLE OF THIOLS IN OXIDATIVE STRESS.Current opinion in toxicology · 2018Article
- Distinct Shift in Beta-Cell Glutaredoxin 5 Expression Is Mediated by Hypoxia and Lipotoxicity BothFrontiers in endocrinology · 2018Article
- Biomarkers of Chronic Acrolein Inhalation Exposure in Mice: Implications for Tobacco Product-Induced Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- Differential expression of islet glutaredoxin 1 and 5 with high reactive oxygen species production in a mouse model of diabesity.PloS one · 2017Article
- Measurement of Reactive Oxygen Species, Reactive Nitrogen Species, and Redox-Dependent Signaling in the Cardiovascular System: A Scientific Statement From the American Heart Association.Circulation research · 2016Review
- Detoxifying Enzymes at the Cross-Roads of Inflammation, Oxidative Stress, and Drug Hypersensitivity: Role of Glutathione Transferase P1-1 and Aldose Reductase.Frontiers in pharmacology · 2016Article
- Biological chemistry and functionality of protein sulfenic acids and related thiol modifications.Free radical research · 2016Review
- Glutathione S-transferase P protects against cyclophosphamide-induced cardiotoxicity in mice.Toxicology and applied pharmacology · 2015Article
- Redox regulation of antioxidants, autophagy, and the response to stress: implications for electrophile therapeutics.Free radical biology & medicine · 2014Review
- Positive oxidative stress in aging and aging-related disease tolerance.Redox biology · 2014Review
- The effect of disease on human cardiac protein expression profiles in paired samples from right and left ventricles.Clinical proteomics · 2014Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Aldose reductase (AR) is a multifunctional enzyme that catalyzes the reduction of glucose and lipid peroxidation-derived aldehydes. During myocardial ischemia, the activity of AR is increased due to the oxidation of its cysteine residues to sulfenic acids. It is not known, however, whether the activated, sulfenic form of the protein (AR-SOH) is converted back to its reduced, unactivated state (AR-SH). We report here that in perfused mouse hearts activation of AR during 15 min of global ischemia is completely reversed by 30 min of reperfusion. During reperfusion, AR-SOH was converted to a mixed disulfide (AR-SSG). Deactivation of AR and the appearance of AR-SSG during reperfusion were delayed in hearts of mice lacking glutathione S-transferase P (GSTP). In vitro, GSTP accelerated glutathiolation and inactivation of AR-SOH. Reduction of AR-SSG to AR-SH was facilitated by glutaredoxin (GRX). Ischemic activation of AR was increased in GRX-null hearts but was attenuated in the hearts of cardiospecific GRX transgenic mice. Incubation of AR-SSG with GRX led to the regeneration of the reduced form of the enzyme. In ischemic cardiospecific AR transgenic hearts, AR was co-immunoprecipitated with GSTP, whereas in reperfused hearts, the association of AR with GRX was increased. These findings suggest that upon reperfusion of the ischemic heart AR-SOH is converted to AR-SSG via GSTP-assisted glutathiolation. AR-SSG is then reduced by GRX to AR-SH. Sequential catalysis by GSTP and GRX may be a general redox switching mechanism that regulates the reduction of protein sulfenic acids to cysteines.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.