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Article: Intermittent hypoxia-induced NF-kB and HO-1 regulation in human endothelial EA.hy926 cells

TitleIntermittent hypoxia-induced NF-kB and HO-1 regulation in human endothelial EA.hy926 cells
Authors
Issue Date2013
Citation
Cell Biochemistry and Biophysics, 2013, v. 66, no. 3, p. 431-441 How to Cite?
AbstractIntermittent hypoxia (IH) is a hallmark feature in obstructive sleep apnea (OSA) which is increasingly recognized as an independent risk factor for atherosclerosis. Oxidative stress, inflammation, and cell apoptosis are major pathological events initiating or accelerating atherogenesis. This study addressed whether IH would affect these proatherogenic factors in endothelial cells and the mechanistic pathways involved. EA.hy926 cells were exposed to intermittent normoxia or IH for different numbers of cycles (32, 64, or 96). IH exposure time-dependently raised cellular GSSG/GSH ratio, increased production of IL-6 and IL-8, and accelerated cell apoptosis and death, concurrent with activation of NF-κB and inhibition of Nrf2/HO-1 pathways. At 64 cycles, inhibition of NF-κB attenuated IH-induced cellular oxidative stress and accumulation of inflammatory cytokines in cell culture medium but aggravated IH-induced cell apoptosis, while stimulation of HO-1 suppressed IH-induced cellular oxidative stress and cell apoptosis without affecting accumulation of inflammatory cytokines in cell culture medium. We demonstrated that early stage of exposure to IH-induced oxidative and inflammatory stresses leading to acceleration of cell apoptosis via NF-κB and Nrf2/HO-1 pathways in endothelial cells, suggesting the potential mechanisms for IH-induced vascular pathogenesis, in resemblance to OSA.
Persistent Identifierhttp://hdl.handle.net/10722/186065
ISSN
2015 Impact Factor: 1.627
2015 SCImago Journal Rankings: 0.598
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHAN, Qen_US
dc.contributor.authorYeung, SCen_US
dc.contributor.authorIp, MSMen_US
dc.contributor.authorMak, JCWen_US
dc.date.accessioned2013-08-20T11:50:27Z-
dc.date.available2013-08-20T11:50:27Z-
dc.date.issued2013en_US
dc.identifier.citationCell Biochemistry and Biophysics, 2013, v. 66, no. 3, p. 431-441en_US
dc.identifier.issn1085-9195-
dc.identifier.urihttp://hdl.handle.net/10722/186065-
dc.description.abstractIntermittent hypoxia (IH) is a hallmark feature in obstructive sleep apnea (OSA) which is increasingly recognized as an independent risk factor for atherosclerosis. Oxidative stress, inflammation, and cell apoptosis are major pathological events initiating or accelerating atherogenesis. This study addressed whether IH would affect these proatherogenic factors in endothelial cells and the mechanistic pathways involved. EA.hy926 cells were exposed to intermittent normoxia or IH for different numbers of cycles (32, 64, or 96). IH exposure time-dependently raised cellular GSSG/GSH ratio, increased production of IL-6 and IL-8, and accelerated cell apoptosis and death, concurrent with activation of NF-κB and inhibition of Nrf2/HO-1 pathways. At 64 cycles, inhibition of NF-κB attenuated IH-induced cellular oxidative stress and accumulation of inflammatory cytokines in cell culture medium but aggravated IH-induced cell apoptosis, while stimulation of HO-1 suppressed IH-induced cellular oxidative stress and cell apoptosis without affecting accumulation of inflammatory cytokines in cell culture medium. We demonstrated that early stage of exposure to IH-induced oxidative and inflammatory stresses leading to acceleration of cell apoptosis via NF-κB and Nrf2/HO-1 pathways in endothelial cells, suggesting the potential mechanisms for IH-induced vascular pathogenesis, in resemblance to OSA.-
dc.languageengen_US
dc.relation.ispartofCell Biochemistry and Biophysicsen_US
dc.titleIntermittent hypoxia-induced NF-kB and HO-1 regulation in human endothelial EA.hy926 cellsen_US
dc.typeArticleen_US
dc.identifier.emailYeung, SC: flag@hkucc.hku.hken_US
dc.identifier.emailIp, MSM: msmip@hku.hken_US
dc.identifier.emailMak, JCW: judymak@hku.hken_US
dc.identifier.authorityIp, MSM=rp00347en_US
dc.identifier.authorityMak, JCW=rp00352en_US
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s12013-012-9491-6-
dc.identifier.pmid23238643-
dc.identifier.hkuros220858en_US
dc.identifier.volume66en_US
dc.identifier.issue3-
dc.identifier.spage431en_US
dc.identifier.epage441en_US
dc.identifier.eissn1559-0283-
dc.identifier.isiWOS:000322526500002-

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