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Conference Paper: Intermittent hypoxia enhances inflammation and oxidative stress in Eahy926 endothelial cells via suppression of HO-1 expression

TitleIntermittent hypoxia enhances inflammation and oxidative stress in Eahy926 endothelial cells via suppression of HO-1 expression
Authors
KeywordsMedical sciences
Respiratory diseases
Issue Date2011
PublisherAmerican Thoracic Society. The Journal's web site is located at http://ajrccm.atsjournals.org
Citation
The 2011 International Conference of the American Thoracic Society (ATS), Denver, CO., 13-18 May 2011. In American Journal of Respiratory and Critical Care Medicine, 2011, v. 183 (Meeting Abstracts), abstract no. A2475 How to Cite?
AbstractRATIONALE: Intermittent hypoxia (IH) is a hallmark feature in obstructive sleep apnea (OSA), which is increasingly recognized as an independent risk factor of atherosclerosis. Although the underlying mechanisms have not been fully understood, inflammation and oxidative stress have been suggested as major pathological events initiating or accelerating atherogenesis. Heme oxygenase-1 (HO-1) plays a regulatory role in the inflammatory response by modulating production of pro-inflammatory cytokines, and its expression is mediated by nuclear translocation of nuclear factor, erythroid 2 related factor 2 (Nrf-2), a transcription factor in response to oxidative stress. This study was to address whether IH would upregulate the expression of pro-inflammatory cytokines via HO-1 expression in endothelial cells in vitro. METHODS: EAhy 926 cells were exposed to intermittent normoxia (IN as control) or IH [a 10-min hypoxia (5% O2) followed by a 5-min normoxia (21% O2) for 64 cycles using the BioSpherix OxyCycler C42 system (BioSpherix, Redfield, NY)]. IL-6 and IL-8 mRNA expressions were measured by RT-PCR, and protein secreted was measured by ELISA. Cellular activities of GSH-related enzymes such as glutathione peroxidase (GPx) and glutathione reductase (GR) were analyzed. Whole cell lysates, cytosolic and nuclear fractions were extracted to perform Western blot for HO-1, Nrf-2, and phospho-ERK. RESULTS: IH increased the production of IL-6 and IL-8 protein without changing the mRNA levels. IH also enhanced the enzyme activities of GPx and GR. On the other hand, IH suppressed HO-1 and Nrf-2 expression, accompanied by the inhibition of ERK phosphorylation. CONCLUSIONS: These data suggest an underlying mechanism for OSA subjects predisposed to atherosclerosis and a potential role of HO-1 in the therapeutic therapy of OSA-related atherosclerosis.
DescriptionPoster Discussion Session - A109 Hypoxia
Persistent Identifierhttp://hdl.handle.net/10722/137792
ISSN
2015 Impact Factor: 13.118
2015 SCImago Journal Rankings: 5.832

 

DC FieldValueLanguage
dc.contributor.authorHan, Qen_US
dc.contributor.authorYeung, SCen_US
dc.contributor.authorIp, MSMen_US
dc.contributor.authorMak, JCWen_US
dc.date.accessioned2011-08-26T14:33:27Z-
dc.date.available2011-08-26T14:33:27Z-
dc.date.issued2011en_US
dc.identifier.citationThe 2011 International Conference of the American Thoracic Society (ATS), Denver, CO., 13-18 May 2011. In American Journal of Respiratory and Critical Care Medicine, 2011, v. 183 (Meeting Abstracts), abstract no. A2475en_US
dc.identifier.issn1073-449X-
dc.identifier.urihttp://hdl.handle.net/10722/137792-
dc.descriptionPoster Discussion Session - A109 Hypoxia-
dc.description.abstractRATIONALE: Intermittent hypoxia (IH) is a hallmark feature in obstructive sleep apnea (OSA), which is increasingly recognized as an independent risk factor of atherosclerosis. Although the underlying mechanisms have not been fully understood, inflammation and oxidative stress have been suggested as major pathological events initiating or accelerating atherogenesis. Heme oxygenase-1 (HO-1) plays a regulatory role in the inflammatory response by modulating production of pro-inflammatory cytokines, and its expression is mediated by nuclear translocation of nuclear factor, erythroid 2 related factor 2 (Nrf-2), a transcription factor in response to oxidative stress. This study was to address whether IH would upregulate the expression of pro-inflammatory cytokines via HO-1 expression in endothelial cells in vitro. METHODS: EAhy 926 cells were exposed to intermittent normoxia (IN as control) or IH [a 10-min hypoxia (5% O2) followed by a 5-min normoxia (21% O2) for 64 cycles using the BioSpherix OxyCycler C42 system (BioSpherix, Redfield, NY)]. IL-6 and IL-8 mRNA expressions were measured by RT-PCR, and protein secreted was measured by ELISA. Cellular activities of GSH-related enzymes such as glutathione peroxidase (GPx) and glutathione reductase (GR) were analyzed. Whole cell lysates, cytosolic and nuclear fractions were extracted to perform Western blot for HO-1, Nrf-2, and phospho-ERK. RESULTS: IH increased the production of IL-6 and IL-8 protein without changing the mRNA levels. IH also enhanced the enzyme activities of GPx and GR. On the other hand, IH suppressed HO-1 and Nrf-2 expression, accompanied by the inhibition of ERK phosphorylation. CONCLUSIONS: These data suggest an underlying mechanism for OSA subjects predisposed to atherosclerosis and a potential role of HO-1 in the therapeutic therapy of OSA-related atherosclerosis.-
dc.languageengen_US
dc.publisherAmerican Thoracic Society. The Journal's web site is located at http://ajrccm.atsjournals.org-
dc.relation.ispartofAmerican Journal of Respiratory and Critical Care Medicineen_US
dc.subjectMedical sciences-
dc.subjectRespiratory diseases-
dc.titleIntermittent hypoxia enhances inflammation and oxidative stress in Eahy926 endothelial cells via suppression of HO-1 expressionen_US
dc.typeConference_Paperen_US
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1073-449X&volume=183&issue=Meeting Abstracts&spage=abstract no. A2475&epage=&date=2011&atitle=Intermittent+hypoxia+enhances+inflammation+and+oxidative+stress+in+Eahy926+endothelial+cells+via+suppression+of+HO-1+expression-
dc.identifier.emailYeung, SC: flag@hkucc.hku.hken_US
dc.identifier.emailIp, MSM: msmip@hku.hken_US
dc.identifier.emailMak, JCW: judithmak@hku.hken_US
dc.identifier.authorityIp, MSM=rp00347en_US
dc.identifier.authorityMak, JCW=rp00352en_US
dc.identifier.hkuros191799en_US
dc.identifier.volume183-
dc.identifier.issueMeeting Abstracts-
dc.description.otherThe 2011 International Conference of the American Thoracic Society (ATS), Denver, CO., 13-18 May 2011. In American Journal of Respiratory and Critical Care Medicine, 2011, v. 183 (Meeting Abstracts), abstract no. A2475-

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