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Conference Paper: Effects of intermittent hypoxia and/or TNF-alpha on E- and A-FABP expression by human aortic endothelial cells in vitro

TitleEffects of intermittent hypoxia and/or TNF-alpha on E- and A-FABP expression by human aortic endothelial cells in vitro
Authors
Issue Date2009
PublisherAmerican Thoracic Society. The Journal's web site is located at http://ajrccm.atsjournals.org
Citation
The International Conference of the American Thoracic Society (ATS) 2009, San Diego, CA., 15-20 May 2010. In American Journal of Respiratory and Critical Care Medicine, 2009, v. 179: A1064 How to Cite?
AbstractRATIONALE: Fatty acid-binding proteins (FABPs) are members of the lipid-binding proteins (LBPs) superfamily, regulating the fatty acid uptake and intercellular transport. Among 9 subtypes identified with tissue-specific distribution, E- and A-FABP have been found to mediate atherosclerosis in animals. Obstructive sleep apnea (OSA) characterized by recurrent intermittent hypoxia (IH), is closely associated with atherosclerosis. On the other hand, TNF-α is a prominent pro-inflammatory cytokine that induces monocyte migration into endothelial cells, thus initiating or accelerating atherosclerosis. This study was to explore the effects of IH and/or TNF-α on E- and A-FABP expression by endothelial cells in vitro. METHODS: Human abdominal aortic endothelial cells (HAAE) were exposed to intermittent normoxia (IN as control) or IH [a 5-min hypoxia (5% O2) followed by a 10-min normoxia (21% O2) for 64 cycles using the BioSpherix OxyCycler C42 system] in the absence or presence of TNF-α. The mRNA levels of E- and A-FABP in HAAE were determined using RT-PCR. RESULTS: IH alone significantly upregulated E- and A-FABP mRNA (1.25-fold and 1.44-fold vs control for E- and A-FABP respectively, p < 0.05; n =4). The combination of TNF-α with IH caused additive effect on elevated mRNA expressions of E- and A-FABP (1.81-fold and 2.4-fold vs control for E- and A-FABP respectively, p < 0.05; n =4). CONCLUSION: We found that IH alone led to upregulation, and to further enhancement of E- and A-FABP expression in presence of TNF-α by endothelial cells. Since elevated circulating TNF-α level has been described in OSA, our data suggests that OSA may be prone to upregulation of E- and A-FABP expression and thus atherosclerosis due to IH and inflammation.
DescriptionA20: Physiological Responses To Intermittent Hypoxia
Persistent Identifierhttp://hdl.handle.net/10722/62345
ISSN
2015 Impact Factor: 13.118
2015 SCImago Journal Rankings: 5.832

 

DC FieldValueLanguage
dc.contributor.authorHan, Qen_HK
dc.contributor.authorYeung, SCen_HK
dc.contributor.authorHo, SPen_HK
dc.contributor.authorIp, MSen_HK
dc.contributor.authorMak, JCen_HK
dc.date.accessioned2010-07-13T03:59:16Z-
dc.date.available2010-07-13T03:59:16Z-
dc.date.issued2009en_HK
dc.identifier.citationThe International Conference of the American Thoracic Society (ATS) 2009, San Diego, CA., 15-20 May 2010. In American Journal of Respiratory and Critical Care Medicine, 2009, v. 179: A1064en_HK
dc.identifier.issn1073-449Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/62345-
dc.descriptionA20: Physiological Responses To Intermittent Hypoxia-
dc.description.abstractRATIONALE: Fatty acid-binding proteins (FABPs) are members of the lipid-binding proteins (LBPs) superfamily, regulating the fatty acid uptake and intercellular transport. Among 9 subtypes identified with tissue-specific distribution, E- and A-FABP have been found to mediate atherosclerosis in animals. Obstructive sleep apnea (OSA) characterized by recurrent intermittent hypoxia (IH), is closely associated with atherosclerosis. On the other hand, TNF-α is a prominent pro-inflammatory cytokine that induces monocyte migration into endothelial cells, thus initiating or accelerating atherosclerosis. This study was to explore the effects of IH and/or TNF-α on E- and A-FABP expression by endothelial cells in vitro. METHODS: Human abdominal aortic endothelial cells (HAAE) were exposed to intermittent normoxia (IN as control) or IH [a 5-min hypoxia (5% O2) followed by a 10-min normoxia (21% O2) for 64 cycles using the BioSpherix OxyCycler C42 system] in the absence or presence of TNF-α. The mRNA levels of E- and A-FABP in HAAE were determined using RT-PCR. RESULTS: IH alone significantly upregulated E- and A-FABP mRNA (1.25-fold and 1.44-fold vs control for E- and A-FABP respectively, p < 0.05; n =4). The combination of TNF-α with IH caused additive effect on elevated mRNA expressions of E- and A-FABP (1.81-fold and 2.4-fold vs control for E- and A-FABP respectively, p < 0.05; n =4). CONCLUSION: We found that IH alone led to upregulation, and to further enhancement of E- and A-FABP expression in presence of TNF-α by endothelial cells. Since elevated circulating TNF-α level has been described in OSA, our data suggests that OSA may be prone to upregulation of E- and A-FABP expression and thus atherosclerosis due to IH and inflammation.-
dc.languageengen_HK
dc.publisherAmerican Thoracic Society. The Journal's web site is located at http://ajrccm.atsjournals.orgen_HK
dc.relation.ispartofAmerican Journal of Respiratory and Critical Care Medicine-
dc.titleEffects of intermittent hypoxia and/or TNF-alpha on E- and A-FABP expression by human aortic endothelial cells in vitroen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1073-449X&volume=179: A1064&spage=&epage=&date=2009&atitle=Effects+of+intermittent+hypoxia+and/or+TNF-alpha+on+E-+and+A-FABP+expression+by+human+aortic+endothelial+cells+in+vitroen_HK
dc.identifier.emailHan, Q: hanqian@hkusua.hku.hken_HK
dc.identifier.emailYeung, SC: h0294069@graduate.hku.hken_HK
dc.identifier.emailHo, SP: spho1@hkucc.hku.hken_HK
dc.identifier.emailIp, MS: msmip@hku.hk-
dc.identifier.emailMak, JC: judymak@HKUCC.hku.hk-
dc.identifier.hkuros171673en_HK
dc.identifier.volume179-
dc.description.otherThe International Conference of the American Thoracic Society (ATS) 2009, San Diego, CA., 15-20 May 2010. In American Journal of Respiratory and Critical Care Medicine, 2009, v. 179: A1064-

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