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Article: The possible role of hydrogen sulfide as a smooth muscle cell proliferation inhibitor in rat cultured cells

TitleThe possible role of hydrogen sulfide as a smooth muscle cell proliferation inhibitor in rat cultured cells
Authors
Issue Date2004
PublisherSpringer Japan. The Journal's web site is located at www.springerlink.com/openurl.asp?genre=journal&issn=0910-8327
Citation
Heart And Vessels, 2004, v. 19 n. 2, p. 75-80 How to Cite?
AbstractHydrogen sulfide (H2S) was recently suggested to be a possible endogenous gasotransmitter in physiological concentration. For the purpose of understanding its possible role in the regulation of the cardiovascular system, we explored the potential effect of H2S on the proliferation of cultured aortic vascular smooth muscle cells (VSMCs) of rats and mitrogen-activated protein kinase (MAPK as a signaling transduction pathway. Vascular smooth muscle cells were cultured in vitro and the cells were divided into six groups: (1) control group, (2) serum group, (3) endothelin group, (4) NaHS group, (5 serum + NaHS group, and (6) endothelin + NaHS group. VSMC proliferation was measured by [3H]thymidine ([3H]TdR) incorporation and MAPK activity in the VSMCs was determined by radioactivity assay. The results showed that endothelin-1 increased VSMC [3H]TdR incorporation 2.39-fold (P < 0.01) and MAPK activity 1.62-fold (P < 0.01), as compared with controls. Hydrogen sulfide at 5 × 10-5mol/l, 1 × 10-4mol/l, and 5 × 10-4 mol/l decreased VSMC [3H]TdR incorporation by 16.8%, 26.60%, and 37.40%, respectively, and reduced MAPK activity by 7.37% (P > 0.05), 23.39%, and 33.57%, respectively (P < 0.01). The results demonstrated that H2S could dose-dependently suppress the proliferation of VSMCs through the MAPK pathway. © Springer-Verlag 2004.
Persistent Identifierhttp://hdl.handle.net/10722/170339
ISSN
2015 Impact Factor: 2.293
2015 SCImago Journal Rankings: 0.709
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDu, Jen_US
dc.contributor.authorHui, Yen_US
dc.contributor.authorCheung, Yen_US
dc.contributor.authorBin, Gen_US
dc.contributor.authorJiang, Hen_US
dc.contributor.authorChen, Xen_US
dc.contributor.authorTang, Cen_US
dc.date.accessioned2012-10-30T06:07:37Z-
dc.date.available2012-10-30T06:07:37Z-
dc.date.issued2004en_US
dc.identifier.citationHeart And Vessels, 2004, v. 19 n. 2, p. 75-80en_US
dc.identifier.issn0910-8327en_US
dc.identifier.urihttp://hdl.handle.net/10722/170339-
dc.description.abstractHydrogen sulfide (H2S) was recently suggested to be a possible endogenous gasotransmitter in physiological concentration. For the purpose of understanding its possible role in the regulation of the cardiovascular system, we explored the potential effect of H2S on the proliferation of cultured aortic vascular smooth muscle cells (VSMCs) of rats and mitrogen-activated protein kinase (MAPK as a signaling transduction pathway. Vascular smooth muscle cells were cultured in vitro and the cells were divided into six groups: (1) control group, (2) serum group, (3) endothelin group, (4) NaHS group, (5 serum + NaHS group, and (6) endothelin + NaHS group. VSMC proliferation was measured by [3H]thymidine ([3H]TdR) incorporation and MAPK activity in the VSMCs was determined by radioactivity assay. The results showed that endothelin-1 increased VSMC [3H]TdR incorporation 2.39-fold (P < 0.01) and MAPK activity 1.62-fold (P < 0.01), as compared with controls. Hydrogen sulfide at 5 × 10-5mol/l, 1 × 10-4mol/l, and 5 × 10-4 mol/l decreased VSMC [3H]TdR incorporation by 16.8%, 26.60%, and 37.40%, respectively, and reduced MAPK activity by 7.37% (P > 0.05), 23.39%, and 33.57%, respectively (P < 0.01). The results demonstrated that H2S could dose-dependently suppress the proliferation of VSMCs through the MAPK pathway. © Springer-Verlag 2004.en_US
dc.languageengen_US
dc.publisherSpringer Japan. The Journal's web site is located at www.springerlink.com/openurl.asp?genre=journal&issn=0910-8327en_US
dc.relation.ispartofHeart and Vesselsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAorta, Thoracic - Cytologyen_US
dc.subject.meshCell Division - Drug Effectsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshEndothelins - Pharmacologyen_US
dc.subject.meshHydrogen Sulfide - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMitogen-Activated Protein Kinase Kinases - Metabolismen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshSignal Transductionen_US
dc.titleThe possible role of hydrogen sulfide as a smooth muscle cell proliferation inhibitor in rat cultured cellsen_US
dc.typeArticleen_US
dc.identifier.emailCheung, Y:xfcheung@hku.hken_US
dc.identifier.authorityCheung, Y=rp00382en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/s00380-003-0743-7en_US
dc.identifier.pmid15042391-
dc.identifier.scopuseid_2-s2.0-1642551072en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-1642551072&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume19en_US
dc.identifier.issue2en_US
dc.identifier.spage75en_US
dc.identifier.epage80en_US
dc.identifier.isiWOS:000220347000004-
dc.publisher.placeJapanen_US
dc.identifier.scopusauthoridDu, J=7402574838en_US
dc.identifier.scopusauthoridHui, Y=16939169300en_US
dc.identifier.scopusauthoridCheung, Y=7202111067en_US
dc.identifier.scopusauthoridBin, G=6601959778en_US
dc.identifier.scopusauthoridJiang, H=7404461596en_US
dc.identifier.scopusauthoridChen, X=8663698000en_US
dc.identifier.scopusauthoridTang, C=7404393937en_US

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