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Article: Hydrogen sulfide inhibits proliferation and release of IL-8 from human airway smooth muscle cells

TitleHydrogen sulfide inhibits proliferation and release of IL-8 from human airway smooth muscle cells
Authors
Issue Date2011
PublisherAmerican Thoracic Society. The Journal's web site is located at http://ajrcmb.atsjournals.org
Citation
American Journal of Respiratory Cell and Molecular Biology, 2011, v. 45 n. 4, p. 746-752 How to Cite?
AbstractHydrogen sulfide (H(2)S) is synthesized intracellularly by the enzymes cystathionine-gamma-lyase and cystathionine-beta-synthase (CBS), and is proposed to be a gasotransmitter with effects in modulating inflammation and cellular proliferation. We determined a role of H(2)S in airway smooth muscle (ASM) function. ASM were removed from resection or transplant donor lungs and were placed in culture. Proliferation of ASM was induced by FCS and the proinflammatory cytokine, IL-1beta. Proliferation of ASM and IL-8 release were measured by bromodeoxyuridine incorporation and ELISA, respectively. Exposure of ASM to H(2)S 'donors' inhibited this proliferation and IL-8 release. Methemoglobin, a scavenger of endogenous H(2)S, increased DNA synthesis induced by FCS and IL-1beta. In addition, methemoglobin increased IL-8 release induced by FCS, but not by IL-1beta, indicating a role for endogenous H(2)S in these systems. Inhibition of CBS, but not cystathionine-gamma-lyase, reversed the inhibitory effect of H(2)S on proliferation and IL-8 release, indicating that this is dependent on CBS. CBS mRNA and protein expression were inhibited by H(2)S donors, and were increased by methemoglobin, indicating that CBS is the main enzyme responsible for endogenous H(2)S production. Finally, we found that exogenous H(2)S inhibited the phosphorylation of extracellular signal-regulated kinase-1/2 and p38, which could represent a mechanism by which H(2)S inhibited cellular proliferation and IL-8 release. In summary, H(2)S production provides a novel mechanism for regulation of ASM proliferation and IL-8 release. Therefore, regulation of H(2)S may represent a novel approach to controlling ASM proliferation and cytokine release that is found in patients with asthma.
Persistent Identifierhttp://hdl.handle.net/10722/192089
ISSN
2015 Impact Factor: 4.082
2015 SCImago Journal Rankings: 1.622
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorPerry, MM-
dc.contributor.authorHui, CK-
dc.contributor.authorWhiteman, M-
dc.contributor.authorWood, ME-
dc.contributor.authorAdcock, I-
dc.contributor.authorKirkham, P-
dc.contributor.authorMichaeloudes, C-
dc.contributor.authorChung, KF-
dc.date.accessioned2013-10-18T08:59:22Z-
dc.date.available2013-10-18T08:59:22Z-
dc.date.issued2011-
dc.identifier.citationAmerican Journal of Respiratory Cell and Molecular Biology, 2011, v. 45 n. 4, p. 746-752-
dc.identifier.issn1044-1549-
dc.identifier.urihttp://hdl.handle.net/10722/192089-
dc.description.abstractHydrogen sulfide (H(2)S) is synthesized intracellularly by the enzymes cystathionine-gamma-lyase and cystathionine-beta-synthase (CBS), and is proposed to be a gasotransmitter with effects in modulating inflammation and cellular proliferation. We determined a role of H(2)S in airway smooth muscle (ASM) function. ASM were removed from resection or transplant donor lungs and were placed in culture. Proliferation of ASM was induced by FCS and the proinflammatory cytokine, IL-1beta. Proliferation of ASM and IL-8 release were measured by bromodeoxyuridine incorporation and ELISA, respectively. Exposure of ASM to H(2)S 'donors' inhibited this proliferation and IL-8 release. Methemoglobin, a scavenger of endogenous H(2)S, increased DNA synthesis induced by FCS and IL-1beta. In addition, methemoglobin increased IL-8 release induced by FCS, but not by IL-1beta, indicating a role for endogenous H(2)S in these systems. Inhibition of CBS, but not cystathionine-gamma-lyase, reversed the inhibitory effect of H(2)S on proliferation and IL-8 release, indicating that this is dependent on CBS. CBS mRNA and protein expression were inhibited by H(2)S donors, and were increased by methemoglobin, indicating that CBS is the main enzyme responsible for endogenous H(2)S production. Finally, we found that exogenous H(2)S inhibited the phosphorylation of extracellular signal-regulated kinase-1/2 and p38, which could represent a mechanism by which H(2)S inhibited cellular proliferation and IL-8 release. In summary, H(2)S production provides a novel mechanism for regulation of ASM proliferation and IL-8 release. Therefore, regulation of H(2)S may represent a novel approach to controlling ASM proliferation and cytokine release that is found in patients with asthma.-
dc.languageeng-
dc.publisherAmerican Thoracic Society. The Journal's web site is located at http://ajrcmb.atsjournals.org-
dc.relation.ispartofAmerican Journal of Respiratory Cell and Molecular Biology-
dc.subject.meshBronchi - drug effects - immunology - metabolism - pathology-
dc.subject.meshCell Proliferation - drug effects-
dc.subject.meshHydrogen Sulfide - metabolism-
dc.subject.meshInterleukin-8 - metabolism-
dc.subject.meshMyocytes, Smooth Muscle - drug effects - immunology - metabolism - pathology-
dc.titleHydrogen sulfide inhibits proliferation and release of IL-8 from human airway smooth muscle cellsen_US
dc.typeArticleen_US
dc.identifier.emailHui, CK: chris.hui@hku.hk-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1165/rcmb.2010-0304OC-
dc.identifier.pmid21297080-
dc.identifier.pmcidPMC3577139-
dc.identifier.scopuseid_2-s2.0-80051927433-
dc.identifier.volume45-
dc.identifier.issue4-
dc.identifier.spage746-
dc.identifier.epage752-
dc.identifier.isiWOS:000299681000010-
dc.publisher.placeUnited States-

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