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Article: Involvement of bcl-2 and caspase-3 in apoptosis induced by cigarette smoke extract in the gastric epithelial cell

TitleInvolvement of bcl-2 and caspase-3 in apoptosis induced by cigarette smoke extract in the gastric epithelial cell
Authors
Issue Date2003
PublisherInforma Healthcare. The Journal's web site is located at http://www.tandf.co.uk/journals/titles/01926233.asp
Citation
Toxicologic Pathology, 2003, v. 31 n. 2, p. 220-226 How to Cite?
AbstractPrevious studies have shown that short-term passive cigarette smoking can increase apoptosis in rat gastric mucosa. However, the mechanism is not yet defined. Chloroform and ethanol extracts were used to investigate whether cigarette smoke could induce apoptosis in a human gastric epithelial cell line (AGS) as well as the roles of bcl-2, caspase-3, and cytochrome c in this process. AGS cell lines were treated with either chloroform extract (CE) or ethanol extract (EE) for 5 hours, and the level of bcl-2, the activity of caspase-3, and the level of cytosolic cytochrome c in these cells were determined. Time course studies on the effects of cigarette smoke extracts (CSEs) on DNA fragmentation and cytochrome c relocalization were also performed. Data showed that only CE induced apoptosis in a dose- and time-dependent manner in AGS cells, along with a decrease of bcl-2 and an increase of caspase-3 activity. Pretreatment with Z-DEVD-FMK (specific inhibitor of caspase-3) dose-dependently blocked the DNA fragmentation induced by the CE. Moreover, CE could time- and dose-dependently increase the level of cytochrome c in the cytoplasm, which might activate caspase-3. In conclusion, CSE triggers apoptosis in AGS cells through the inhibition of bcl-2 and the activation of a mitochondria-related pathway.
Persistent Identifierhttp://hdl.handle.net/10722/88706
ISSN
2015 Impact Factor: 2.197
2015 SCImago Journal Rankings: 1.070
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, HYen_HK
dc.contributor.authorShin, VYen_HK
dc.contributor.authorLeung, SYen_HK
dc.contributor.authorYuen, STen_HK
dc.contributor.authorCho, CHen_HK
dc.date.accessioned2010-09-06T09:46:54Z-
dc.date.available2010-09-06T09:46:54Z-
dc.date.issued2003en_HK
dc.identifier.citationToxicologic Pathology, 2003, v. 31 n. 2, p. 220-226en_HK
dc.identifier.issn0192-6233en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88706-
dc.description.abstractPrevious studies have shown that short-term passive cigarette smoking can increase apoptosis in rat gastric mucosa. However, the mechanism is not yet defined. Chloroform and ethanol extracts were used to investigate whether cigarette smoke could induce apoptosis in a human gastric epithelial cell line (AGS) as well as the roles of bcl-2, caspase-3, and cytochrome c in this process. AGS cell lines were treated with either chloroform extract (CE) or ethanol extract (EE) for 5 hours, and the level of bcl-2, the activity of caspase-3, and the level of cytosolic cytochrome c in these cells were determined. Time course studies on the effects of cigarette smoke extracts (CSEs) on DNA fragmentation and cytochrome c relocalization were also performed. Data showed that only CE induced apoptosis in a dose- and time-dependent manner in AGS cells, along with a decrease of bcl-2 and an increase of caspase-3 activity. Pretreatment with Z-DEVD-FMK (specific inhibitor of caspase-3) dose-dependently blocked the DNA fragmentation induced by the CE. Moreover, CE could time- and dose-dependently increase the level of cytochrome c in the cytoplasm, which might activate caspase-3. In conclusion, CSE triggers apoptosis in AGS cells through the inhibition of bcl-2 and the activation of a mitochondria-related pathway.en_HK
dc.languageengen_HK
dc.publisherInforma Healthcare. The Journal's web site is located at http://www.tandf.co.uk/journals/titles/01926233.aspen_HK
dc.relation.ispartofToxicologic Pathologyen_HK
dc.rightsToxicologic Pathology. Copyright © Informa Healthcare.en_HK
dc.subject.meshAdenocarcinomaen_HK
dc.subject.meshApoptosis - drug effectsen_HK
dc.subject.meshCaspase 3en_HK
dc.subject.meshCaspases - metabolismen_HK
dc.subject.meshCytochrome c Group - metabolismen_HK
dc.subject.meshDNA Fragmentationen_HK
dc.subject.meshDose-Response Relationship, Drugen_HK
dc.subject.meshEpithelial Cells - drug effects - enzymology - pathologyen_HK
dc.subject.meshFlow Cytometryen_HK
dc.subject.meshGastric Mucosa - drug effects - enzymology - pathologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshL-Lactate Dehydrogenase - metabolismen_HK
dc.subject.meshProto-Oncogene Proteins c-bcl-2 - metabolismen_HK
dc.subject.meshSmoke - adverse effectsen_HK
dc.subject.meshStomach Neoplasmsen_HK
dc.subject.meshTobacco - adverse effects - chemistryen_HK
dc.subject.meshTumor Cells, Cultureden_HK
dc.titleInvolvement of bcl-2 and caspase-3 in apoptosis induced by cigarette smoke extract in the gastric epithelial cellen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0192-6233&volume=31 no 2&spage=220&epage=226&date=2003&atitle=Involvement+of+bcl-2+and+Caspase-3+in+Apoptosis+Induced+by+Cigarette+Smoke+Extract+in+the+Gastric+Epithelial+Cellen_HK
dc.identifier.emailLeung, SY:suetyi@hkucc.hku.hken_HK
dc.identifier.authorityLeung, SY=rp00359en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1080/01926230309804en_HK
dc.identifier.pmid12696583-
dc.identifier.scopuseid_2-s2.0-0037348679en_HK
dc.identifier.hkuros92197en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037348679&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume31en_HK
dc.identifier.issue2en_HK
dc.identifier.spage220en_HK
dc.identifier.epage226en_HK
dc.identifier.isiWOS:000181175500009-
dc.publisher.placeUnited Statesen_HK

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