| Inducible hydrogen sulfide synthesis in chondrocytes and mesenchymal progenitor cells: is h(2) S a novel cytoprotective mediator in the inflamed joint? | |
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MedLine Citation:
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PMID: 21679296 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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OBJECTIVE: Hydrogen sulfide (H(2) S) has recently been proposed as an endogenous mediator of inflammation and is present in human synovial fluid. The present study determined whether primary human articular chondrocytes (HAC) and mesenchymal progenitor cells (MPC) could synthesize H(2) S in response to pro-inflammatory cytokines relevant to human arthropathies and to determine the cellular responses to endogenous and pharmacological H(2) S. METHODS: HAC and MPC were exposed to IL-1β, IL-6, TNF-α and LPS. The expression and enzymatic activity of the H(2) S synthesizing enzymes cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CSE) were determined by western blot and zinc-trap spectrophotometry respectively. Cellular oxidative stress was induced by H(2) O(2) , the peroxynitrite donor SIN-1 and 4-hydroxynonenal (4-HNE). Cell death was assessed by MTT and LDH assays. Mitochondrial membrane potential (ΔΨm) was determined in situ by flow cytometry. Endogenous H(2) S synthesis was inhibited by siRNA-mediated knockdown of CSE and CBS and pharmacological inhibitors D,L-propargylglycine and aminoxyacetate respectively. Exogenous H(2) S was generated using GYY4137. RESULTS: Under basal conditions HAC and MPC expressed CBS and CSE and synthesized H(2) S in a CBS-dependent manner whereas CSE expression and activity was induced by treatment of cells with IL-1β, TNF-α, IL-6 or LPS. Oxidative stress induced cell death was significantly inhibited by GYY4137 treatment but increased by pharmacological inhibition of H(2) S synthesis or by CBS/CSE-siRNA treatment. CONCLUSIONS: These data suggest CSE is an inducible source of H(2) S in cultured HAC and MPC. H(2) S may represent a novel endogenous mechanism of cytoprotection in the inflamed joint, suggesting a potential opportunity for therapeutic intervention. |
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Authors:
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Bridget Fox; Jan-Thorsten Schantz; Richard Haigh; Mark E Wood; Phillip K Moore; Nick Viner; Jeremy P E Spencer; Paul G Winyard; Matthew Whiteman |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-6-17 |
Journal Detail:
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Title: Journal of cellular and molecular medicine Volume: - ISSN: 1582-4934 ISO Abbreviation: - Publication Date: 2011 Jun |
Date Detail:
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Created Date: 2011-6-17 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101083777 Medline TA: J Cell Mol Med Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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© 2011 The Authors Journal of Cellular and Molecular Medicine © 2011 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd. |
Affiliation:
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Peninsula Medical School, University of Exeter, St. Luke's Campus, Magdalen Road, Exeter, Devon, England Department of Plastic, Reconstructive and Handsurgery, Klinikum rechts der Isar, Technische Universität München, 80333 München, Germany Division of Plastic Surgery and Bioengineering, National University of Singapore, Singapore 119077 Department of Rheumatology, Royal Devon and Exeter Hospital Trust, Barrack Road, Exeter, Devon, England Biosciences, College of Life and Environmental Sciences of Biosciences, University of Exeter, Streatham Campus, Prince of Wales Road, Exeter, Devon, England Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, 8 Medical Drive, Singapore 119260 Department of Rheumatology, Torbay Hospital, Torbay, Devon, England Department of Chemistry and Food Biosciences, University of Reading, Whiteknights, Berkshire, England Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597. |
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