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Article: Expression of HIF-1α, VEGF and VEGF receptors in the carotid body of chronically hypoxic rat

TitleExpression of HIF-1α, VEGF and VEGF receptors in the carotid body of chronically hypoxic rat
Authors
KeywordsCarotid body, hypoxia, protein expression
Chemoreceptors, carotid body
Control of breathing, hypoxia, carotid body
Hypoxia, carotid body, HIF-1α, VEGF
Mammals, rat
Mediators, HIF-1α
Mediators, VEGF
Receptors, VEGF
Issue Date2003
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/resphysiol
Citation
Respiratory Physiology And Neurobiology, 2003, v. 138 n. 2-3, p. 143-154 How to Cite?
AbstractWe examined the protein expression and localization of HIF-1α, VEGF, VEGF receptors in the carotid body (CB) of rats breathing 10% inspired oxygen for up to 4 weeks. The immunoreactivity (IR) of HIF-1α was distributed numerously in the nuclei of glomus (type-I) and other cells since hypoxia for 1 day, but was faint and scattered in the normoxic CBs. Cytoplasmic staining of the VEGF was intense in glomus cells of the hypoxic but not the normoxic group. The IR levels of HIF-1α and VEGF reached plateau at 4 weeks, and the IRs of VEGFR-1 and VEGFR-2 were strongly positive in the hypoxic group. Yet, the expression of VEGFR-1-IR was mild, whereas the VEGFR-2-IR was intense in normoxic CBs, suggesting an upregulation of VEGFR-1 but not VEGFR-2 in hypoxia. Hence, HIF-1 may activate the expression of VEGF and VEGFR-1 in the CB and the expression of VEGF in the chemoreceptors may play a paracrine role in the vascular remodeling during chronic hypoxia. © 2003 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/149622
ISSN
2015 Impact Factor: 1.773
2015 SCImago Journal Rankings: 0.923
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTipoe, GLen_HK
dc.contributor.authorFung, MLen_HK
dc.date.accessioned2012-06-26T05:56:11Z-
dc.date.available2012-06-26T05:56:11Z-
dc.date.issued2003en_HK
dc.identifier.citationRespiratory Physiology And Neurobiology, 2003, v. 138 n. 2-3, p. 143-154en_HK
dc.identifier.issn1569-9048en_HK
dc.identifier.urihttp://hdl.handle.net/10722/149622-
dc.description.abstractWe examined the protein expression and localization of HIF-1α, VEGF, VEGF receptors in the carotid body (CB) of rats breathing 10% inspired oxygen for up to 4 weeks. The immunoreactivity (IR) of HIF-1α was distributed numerously in the nuclei of glomus (type-I) and other cells since hypoxia for 1 day, but was faint and scattered in the normoxic CBs. Cytoplasmic staining of the VEGF was intense in glomus cells of the hypoxic but not the normoxic group. The IR levels of HIF-1α and VEGF reached plateau at 4 weeks, and the IRs of VEGFR-1 and VEGFR-2 were strongly positive in the hypoxic group. Yet, the expression of VEGFR-1-IR was mild, whereas the VEGFR-2-IR was intense in normoxic CBs, suggesting an upregulation of VEGFR-1 but not VEGFR-2 in hypoxia. Hence, HIF-1 may activate the expression of VEGF and VEGFR-1 in the CB and the expression of VEGF in the chemoreceptors may play a paracrine role in the vascular remodeling during chronic hypoxia. © 2003 Elsevier B.V. All rights reserved.en_HK
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/resphysiolen_HK
dc.relation.ispartofRespiratory Physiology and Neurobiologyen_HK
dc.rightsRespiratory Physiology & Neurobiology. Copyright © Elsevier BV.-
dc.subjectCarotid body, hypoxia, protein expressionen_HK
dc.subjectChemoreceptors, carotid bodyen_HK
dc.subjectControl of breathing, hypoxia, carotid bodyen_HK
dc.subjectHypoxia, carotid body, HIF-1α, VEGFen_HK
dc.subjectMammals, raten_HK
dc.subjectMediators, HIF-1αen_HK
dc.subjectMediators, VEGFen_HK
dc.subjectReceptors, VEGFen_HK
dc.titleExpression of HIF-1α, VEGF and VEGF receptors in the carotid body of chronically hypoxic raten_HK
dc.typeArticleen_HK
dc.identifier.emailTipoe, GL: tgeorge@hkucc.hku.hken_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.authorityTipoe, GL=rp00371en_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S1569-9048(03)00188-5en_HK
dc.identifier.scopuseid_2-s2.0-0242607014en_HK
dc.identifier.hkuros85067-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0242607014&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume138en_HK
dc.identifier.issue2-3en_HK
dc.identifier.spage143en_HK
dc.identifier.epage154en_HK
dc.identifier.isiWOS:000186784500002-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridTipoe, GL=7003550610en_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK

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