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Article: Nicotine suppresses gastric wound repair via the inhibition of polyamine and K+ channel expression

TitleNicotine suppresses gastric wound repair via the inhibition of polyamine and K+ channel expression
Authors
KeywordsCell migration
Cell proliferation
K+ channel
Nicotine
Nicotine receptor
Ornithine decarboxylase
Wound healing
Issue Date2002
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejphar
Citation
European Journal Of Pharmacology, 2002, v. 444 n. 1-2, p. 115-121 How to Cite?
AbstractNicotine is one of the most representative components in cigarette smoke leading to gastric ulceration. Both ornithine decarboxylase and potassium ion (K+) channels are essential for cell growth and wound repair. The aim of the present study is to elucidate the causative relationship of these two factors during wound healing and the influence of nicotine on this healing process in rat gastric mucosal epithelial cells (RGM-1). Nicotine markedly inhibited cell migration and proliferation in RGM-1 cells. The latter effect was significantly antagonized by a nicotinic receptor blocker, mecamylamine. Nicotine also suppressed ornithine decarboxylase activity significantly. Our data showed that inhibition of cell proliferation and ornithine decarboxylase activity by nicotine was accompanied with a reduction in K+ channel protein expression, all of which were significantly alleviated by spermidine pretreatment. These results suggested that there was a cause/effect link between ornithine decarboxylase and K+ channel on wound repair. Nicotine in cigarette smoke inhibited this healing process and delayed wound repair in gastric epithelial cells. © 2002 Published by Elsevier Science B.V.
Persistent Identifierhttp://hdl.handle.net/10722/80282
ISSN
2015 Impact Factor: 2.73
2015 SCImago Journal Rankings: 1.115
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShin, VYen_HK
dc.contributor.authorLiu, ESLen_HK
dc.contributor.authorKoo, MWLen_HK
dc.contributor.authorLuo, JCen_HK
dc.contributor.authorSo, WHLen_HK
dc.contributor.authorCho, CHen_HK
dc.date.accessioned2010-09-06T08:04:34Z-
dc.date.available2010-09-06T08:04:34Z-
dc.date.issued2002en_HK
dc.identifier.citationEuropean Journal Of Pharmacology, 2002, v. 444 n. 1-2, p. 115-121en_HK
dc.identifier.issn0014-2999en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80282-
dc.description.abstractNicotine is one of the most representative components in cigarette smoke leading to gastric ulceration. Both ornithine decarboxylase and potassium ion (K+) channels are essential for cell growth and wound repair. The aim of the present study is to elucidate the causative relationship of these two factors during wound healing and the influence of nicotine on this healing process in rat gastric mucosal epithelial cells (RGM-1). Nicotine markedly inhibited cell migration and proliferation in RGM-1 cells. The latter effect was significantly antagonized by a nicotinic receptor blocker, mecamylamine. Nicotine also suppressed ornithine decarboxylase activity significantly. Our data showed that inhibition of cell proliferation and ornithine decarboxylase activity by nicotine was accompanied with a reduction in K+ channel protein expression, all of which were significantly alleviated by spermidine pretreatment. These results suggested that there was a cause/effect link between ornithine decarboxylase and K+ channel on wound repair. Nicotine in cigarette smoke inhibited this healing process and delayed wound repair in gastric epithelial cells. © 2002 Published by Elsevier Science B.V.en_HK
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejpharen_HK
dc.relation.ispartofEuropean Journal of Pharmacologyen_HK
dc.rightsEuropean Journal of Pharmacology. Copyright © Elsevier BV.en_HK
dc.subjectCell migrationen_HK
dc.subjectCell proliferationen_HK
dc.subjectK+ channelen_HK
dc.subjectNicotineen_HK
dc.subjectNicotine receptoren_HK
dc.subjectOrnithine decarboxylaseen_HK
dc.subjectWound healingen_HK
dc.titleNicotine suppresses gastric wound repair via the inhibition of polyamine and K+ channel expressionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0014-2999&volume=444&spage=115&epage=121&date=2002&atitle=Nicotine+suppresses+gastric+wound+repair+via+the+inhibition+of+polyamine+and+K++channel+expressionen_HK
dc.identifier.emailKoo, MWL: wlkoo@hku.hken_HK
dc.identifier.authorityKoo, MWL=rp00233en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0014-2999(02)01610-2en_HK
dc.identifier.pmid12191590-
dc.identifier.scopuseid_2-s2.0-0037165831en_HK
dc.identifier.hkuros73765en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037165831&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume444en_HK
dc.identifier.issue1-2en_HK
dc.identifier.spage115en_HK
dc.identifier.epage121en_HK
dc.identifier.isiWOS:000176636300015-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridShin, VY=7003491170en_HK
dc.identifier.scopusauthoridLiu, ESL=7202240071en_HK
dc.identifier.scopusauthoridKoo, MWL=7004550899en_HK
dc.identifier.scopusauthoridLuo, JC=7404182407en_HK
dc.identifier.scopusauthoridSo, WHL=7004974020en_HK
dc.identifier.scopusauthoridCho, CH=7403100461en_HK

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