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Conference Paper: NF-kB protects RAT ARL-6 hepatocellular carcinoma cells against hydrogen peroxide-induced apoptosis

TitleNF-kB protects RAT ARL-6 hepatocellular carcinoma cells against hydrogen peroxide-induced apoptosis
Authors
Issue Date2005
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/jhep
Citation
The 40th Annual Meeting of the European Association for the study of the Liver, Paris, France, 13-17 April 2005. In Journal of Hepatology, 2005, v. 42 n. Suppl. 2, p. 140 Abstract no. 379 How to Cite?
AbstractBackground and Aims: Refractoriness of some turnouts to apoptosis has been related to over-expression of NF-kB, but NF-kB inhibition call also promote apoptosis in several cell types. We compared NF-kB activation profiles between normal rat hepatocytes and ARL-6 tat hepatocellular carcinoma (HCC) cells exposed to hydrogen peroxide (H202). We then examined whether NF-kB activation could explain tile observed resistance of ARL-6 cells to HAOA-induced apoptosis by blocking NF-kB activation with adenovirus-mediated mutant (non-degradable) IkBa (mlkB a). We also studied tile effects of NF-kI3 on cell proliferation. Methods: Hepatocytes is isolated from male Wistar rats by collagenase perfusion were established in primary culture in DMEM. ARL-6 cells were cultured in DMEM supplemented with 10% heat-inactivated fetal bovine serum. Inhibition of NF-kB was achieved by infecting cultured ARL-6 cells with mlkBa (or b-sat for controls) for 24h. Infection efficiency was determined by X-gut staining. Cytotoxicity was determined by WST-1 assay. NF-!d3 translocation was determined by Western blot and iraraunofluorescence microscopy, and NF-kB DNA binding by electrophoretic mobility shift, assay (EMSA); cell proliferation was by [H3]- thymidine incorporation. Apoptosis was detected by H-33342 fluorescent microscopy, scanning electron microscopy, and TUNEL assay. Protein expression was measured by Western blotting. Results: At low concentrations, H;O; induced more apoptosis in primary hepatocytes than in ARL-6 cells, and was associated with greater NF-kB activation. In ARL-6 cells, nuclear translocation of NF-kB took place within 2h of administering HAO 2 and remained prominent at 36h. Inhibition of NF-kB by rnIkBa sensitized ARL-6 cells to HAOA-induced apoptosis, but cell proliferation was minimally suppressed. Conelusious: Hepatocytes are exquisitely sensitive to HAOA-induced apoptosis and relatively insensitive to NF-kB activation. In contrast, ARL-6 cells are refractory to apoptosis after exposure to low doses of H202, and this is associated with NF-kB activation. Sustained NF-kB activation in these HCC cells may protect them against apoptosis produced by physiological levels of oxidative stress. Conversely, NF-kB inhibition sensitises ARL-6 cells to oxidative stress-induced apoptosis.
Persistent Identifierhttp://hdl.handle.net/10722/101090
ISSN
2015 Impact Factor: 10.59
2015 SCImago Journal Rankings: 4.570

 

DC FieldValueLanguage
dc.contributor.authorQiao, Len_HK
dc.contributor.authorYu, Jen_HK
dc.contributor.authorFrancisco, Ren_HK
dc.contributor.authorDent, Pen_HK
dc.contributor.authorFarrell, G-
dc.date.accessioned2010-09-25T19:35:34Z-
dc.date.available2010-09-25T19:35:34Z-
dc.date.issued2005en_HK
dc.identifier.citationThe 40th Annual Meeting of the European Association for the study of the Liver, Paris, France, 13-17 April 2005. In Journal of Hepatology, 2005, v. 42 n. Suppl. 2, p. 140 Abstract no. 379-
dc.identifier.issn0168-8278en_HK
dc.identifier.urihttp://hdl.handle.net/10722/101090-
dc.description.abstractBackground and Aims: Refractoriness of some turnouts to apoptosis has been related to over-expression of NF-kB, but NF-kB inhibition call also promote apoptosis in several cell types. We compared NF-kB activation profiles between normal rat hepatocytes and ARL-6 tat hepatocellular carcinoma (HCC) cells exposed to hydrogen peroxide (H202). We then examined whether NF-kB activation could explain tile observed resistance of ARL-6 cells to HAOA-induced apoptosis by blocking NF-kB activation with adenovirus-mediated mutant (non-degradable) IkBa (mlkB a). We also studied tile effects of NF-kI3 on cell proliferation. Methods: Hepatocytes is isolated from male Wistar rats by collagenase perfusion were established in primary culture in DMEM. ARL-6 cells were cultured in DMEM supplemented with 10% heat-inactivated fetal bovine serum. Inhibition of NF-kB was achieved by infecting cultured ARL-6 cells with mlkBa (or b-sat for controls) for 24h. Infection efficiency was determined by X-gut staining. Cytotoxicity was determined by WST-1 assay. NF-!d3 translocation was determined by Western blot and iraraunofluorescence microscopy, and NF-kB DNA binding by electrophoretic mobility shift, assay (EMSA); cell proliferation was by [H3]- thymidine incorporation. Apoptosis was detected by H-33342 fluorescent microscopy, scanning electron microscopy, and TUNEL assay. Protein expression was measured by Western blotting. Results: At low concentrations, H;O; induced more apoptosis in primary hepatocytes than in ARL-6 cells, and was associated with greater NF-kB activation. In ARL-6 cells, nuclear translocation of NF-kB took place within 2h of administering HAO 2 and remained prominent at 36h. Inhibition of NF-kB by rnIkBa sensitized ARL-6 cells to HAOA-induced apoptosis, but cell proliferation was minimally suppressed. Conelusious: Hepatocytes are exquisitely sensitive to HAOA-induced apoptosis and relatively insensitive to NF-kB activation. In contrast, ARL-6 cells are refractory to apoptosis after exposure to low doses of H202, and this is associated with NF-kB activation. Sustained NF-kB activation in these HCC cells may protect them against apoptosis produced by physiological levels of oxidative stress. Conversely, NF-kB inhibition sensitises ARL-6 cells to oxidative stress-induced apoptosis.-
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/jhepen_HK
dc.relation.ispartofJournal of Hepatologyen_HK
dc.rightsJournal of Hepatology. Copyright © Elsevier BV.en_HK
dc.titleNF-kB protects RAT ARL-6 hepatocellular carcinoma cells against hydrogen peroxide-induced apoptosisen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0168-8278&volume=&spage=&epage=&date=2005&atitle=NF-κB+protects+rat+ARL-6+hepatocellular+carcinoma+cells+against+hydrogen+peroxide-induced+apoptosis.en_HK
dc.identifier.emailQiao, L: lq8688@hotmail.comen_HK
dc.identifier.authorityQiao, L=rp00513en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0168-8278(05)81791-X-
dc.identifier.hkuros132423en_HK

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