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Article: Redistribution of cytochrome C is not an essential requirement in C2-ceramide induced apoptosis in HL-60 cells

TitleRedistribution of cytochrome C is not an essential requirement in C2-ceramide induced apoptosis in HL-60 cells
Authors
Issue Date1999
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie
Citation
Life Sciences, 1999, v. 65 n. 10, p. 1715-1723 How to Cite?
Abstractbcl-2 has been shown to enhance cell survival by inhibiting apoptosis. The present study investigates the potential role of bcl-2 on apoptosis in HL-60 cells induced by different agents. HL-60/bcl-2 and control HL-60/neo cells were obtained by transfection of bcl-2 cDNA or the neomycin-resistant gene, respectively. Staurosporine (STS) promoted DNA fragmentation dose-dependently in the 6 h exposure assay while C2-ceramide was relatively slow in the induction of apoptosis (~ 40% after 24 h) and required higher concentrations (> 20 μM). Caspases inhibitors, Ac-YVAD-cmk (100 μM) and zVAD-fmk (20 μM) had no effect on DNA fragmentation themselves. However, they blocked C2-ceramide-induced caspase-3 cleavage and apoptosis, but not the release of cytochrome c from the mitochondria. In addition, we found that both Ac-YVAD-cmk and zVAD-fmk failed to protect STS-induced apoptosis in HL-60 cells. Overexpression of bcl-2 inhibited STS and C2-ceramide induced cytochrome c redistribution, caspase-3 activation and apoptosis. These results suggest a protective role of bcl-2 in the regulation of apoptosis and cytochrome c release is unlikely to be involved in the final common pathway in apoptosis.
Persistent Identifierhttp://hdl.handle.net/10722/224112
ISSN
2015 Impact Factor: 2.685
2015 SCImago Journal Rankings: 1.056

 

DC FieldValueLanguage
dc.contributor.authorZhang, QH-
dc.contributor.authorSheng, HP-
dc.contributor.authorLoh, TT-
dc.date.accessioned2016-03-24T02:18:23Z-
dc.date.available2016-03-24T02:18:23Z-
dc.date.issued1999-
dc.identifier.citationLife Sciences, 1999, v. 65 n. 10, p. 1715-1723-
dc.identifier.issn0024-3205-
dc.identifier.urihttp://hdl.handle.net/10722/224112-
dc.description.abstractbcl-2 has been shown to enhance cell survival by inhibiting apoptosis. The present study investigates the potential role of bcl-2 on apoptosis in HL-60 cells induced by different agents. HL-60/bcl-2 and control HL-60/neo cells were obtained by transfection of bcl-2 cDNA or the neomycin-resistant gene, respectively. Staurosporine (STS) promoted DNA fragmentation dose-dependently in the 6 h exposure assay while C2-ceramide was relatively slow in the induction of apoptosis (~ 40% after 24 h) and required higher concentrations (> 20 μM). Caspases inhibitors, Ac-YVAD-cmk (100 μM) and zVAD-fmk (20 μM) had no effect on DNA fragmentation themselves. However, they blocked C2-ceramide-induced caspase-3 cleavage and apoptosis, but not the release of cytochrome c from the mitochondria. In addition, we found that both Ac-YVAD-cmk and zVAD-fmk failed to protect STS-induced apoptosis in HL-60 cells. Overexpression of bcl-2 inhibited STS and C2-ceramide induced cytochrome c redistribution, caspase-3 activation and apoptosis. These results suggest a protective role of bcl-2 in the regulation of apoptosis and cytochrome c release is unlikely to be involved in the final common pathway in apoptosis.-
dc.languageeng-
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie-
dc.relation.ispartofLife Sciences-
dc.subject.meshApoptosis - drug effects-
dc.subject.meshCytochrome C Group - antagonists & inhibitors - metabolism - secretion-
dc.subject.meshHL-60 Cells - cytology - drug effects - enzymology-
dc.subject.meshSodium Dodecyl Sulfate - pharmacology-
dc.subject.meshSphingosine - analogs & derivatives - antagonists & inhibitors/toxicity-
dc.titleRedistribution of cytochrome C is not an essential requirement in C2-ceramide induced apoptosis in HL-60 cells-
dc.typeArticle-
dc.identifier.emailSheng, HP: hpsheng@hkucc.hku.hk-
dc.identifier.emailLoh, TT: ttloh@hkucc.hku.hk-
dc.identifier.doi10.1016/S0024-3205(99)00420-8-
dc.identifier.pmid10573189-
dc.identifier.scopuseid_2-s2.0-0033543679-
dc.identifier.hkuros53499-
dc.identifier.volume65-
dc.identifier.issue10-
dc.identifier.spage1715-
dc.identifier.epage1723-
dc.publisher.placeUnited States-

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