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Article: Chronic hypoxia upregulates the expression and function of proinflammatory cytokines in the rat carotid body

TitleChronic hypoxia upregulates the expression and function of proinflammatory cytokines in the rat carotid body
Authors
KeywordsCarotid body
Chemoreceptor
Chronic hypoxia
Inflammation
Interleukin
Issue Date2008
PublisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00418/index.htm
Citation
Histochemistry And Cell Biology, 2008, v. 130 n. 3, p. 549-559 How to Cite?
AbstractThe structure and function of the carotid body are greatly altered during chronic hypoxia. Recent studies showed the expression of interleukin (IL)-1 receptor and IL-6 receptor in the carotid body, suggesting a role of proinflammatory cytokines in the chemoreceptor function. The present study aimed to examine the hypothesis that the expression of pro-inflammatory cytokines, namely IL-1β, IL-6 and tumor necrosis factor (TNF)α, plays a role in the rat carotid body in chronic hypoxia. Levels of the mRNA expression of the cytokines and their receptors IL-1r1, gp130 and TNFr1, were significantly increased in the carotid body of hypoxic rats when compared with the normoxic control. Immunohistochemistry showed that the expressions of cytokines and receptors were localized in the lobules of chemosensitive glomus cells containing tyrosine hydroxylase. There were significantly more positive-staining cells in the hypoxic groups with treatment for 3, 7 and 28 days than those of the normoxic controls. Application of exogenous cytokines (0.1 nM) elevated intracellular calcium ([Ca 2+] i) responses to acute hypoxia in the dissociated fura-2-loaded glomus cells. The increased [Ca 2+] i response in the hypoxic group was significantly greater than that of the normoxic group. Moreover, the gene transcripts of inflammatory mediator inducible nitric oxide synthase and chemokines (MCP-1, CCR2, MIP-1α, and ICAM-1) were increased in the carotid body of hypoxic rats. Collectively, results suggest that the increased expressions of proinflammatory cytokines play a functional role in the carotid body with local inflammation during chronic hypoxia. © 2008 Springer-Verlag.
Persistent Identifierhttp://hdl.handle.net/10722/58236
ISSN
2015 Impact Factor: 2.78
2015 SCImago Journal Rankings: 1.287
ISI Accession Number ID
Funding AgencyGrant Number
University of Hong Kong
Council, Hong Kong
Funding Information:

We thank Mr W. B. Wong and Ms K. M. Leung for their technical assistance. This work was supported by research grants from the University of Hong Kong and the Research Grants Council, Hong Kong.

References

 

DC FieldValueLanguage
dc.contributor.authorLam, SYen_HK
dc.contributor.authorTipoe, GLen_HK
dc.contributor.authorLiong, ECen_HK
dc.contributor.authorFung, MLen_HK
dc.date.accessioned2010-05-31T03:26:22Z-
dc.date.available2010-05-31T03:26:22Z-
dc.date.issued2008en_HK
dc.identifier.citationHistochemistry And Cell Biology, 2008, v. 130 n. 3, p. 549-559en_HK
dc.identifier.issn0948-6143en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58236-
dc.description.abstractThe structure and function of the carotid body are greatly altered during chronic hypoxia. Recent studies showed the expression of interleukin (IL)-1 receptor and IL-6 receptor in the carotid body, suggesting a role of proinflammatory cytokines in the chemoreceptor function. The present study aimed to examine the hypothesis that the expression of pro-inflammatory cytokines, namely IL-1β, IL-6 and tumor necrosis factor (TNF)α, plays a role in the rat carotid body in chronic hypoxia. Levels of the mRNA expression of the cytokines and their receptors IL-1r1, gp130 and TNFr1, were significantly increased in the carotid body of hypoxic rats when compared with the normoxic control. Immunohistochemistry showed that the expressions of cytokines and receptors were localized in the lobules of chemosensitive glomus cells containing tyrosine hydroxylase. There were significantly more positive-staining cells in the hypoxic groups with treatment for 3, 7 and 28 days than those of the normoxic controls. Application of exogenous cytokines (0.1 nM) elevated intracellular calcium ([Ca 2+] i) responses to acute hypoxia in the dissociated fura-2-loaded glomus cells. The increased [Ca 2+] i response in the hypoxic group was significantly greater than that of the normoxic group. Moreover, the gene transcripts of inflammatory mediator inducible nitric oxide synthase and chemokines (MCP-1, CCR2, MIP-1α, and ICAM-1) were increased in the carotid body of hypoxic rats. Collectively, results suggest that the increased expressions of proinflammatory cytokines play a functional role in the carotid body with local inflammation during chronic hypoxia. © 2008 Springer-Verlag.en_HK
dc.languageengen_HK
dc.publisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00418/index.htmen_HK
dc.relation.ispartofHistochemistry and Cell Biologyen_HK
dc.subjectCarotid bodyen_HK
dc.subjectChemoreceptoren_HK
dc.subjectChronic hypoxiaen_HK
dc.subjectInflammationen_HK
dc.subjectInterleukinen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAnoxia - genetics - metabolismen_HK
dc.subject.meshCalcium - metabolismen_HK
dc.subject.meshCarotid Body - metabolismen_HK
dc.subject.meshChronic Diseaseen_HK
dc.subject.meshCytokines - genetics - metabolismen_HK
dc.subject.meshMaleen_HK
dc.subject.meshNitric Oxide Synthase Type II - genetics - metabolismen_HK
dc.subject.meshRNA, Messenger - geneticsen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshReceptors, Cytokine - genetics - metabolismen_HK
dc.subject.meshUp-Regulationen_HK
dc.titleChronic hypoxia upregulates the expression and function of proinflammatory cytokines in the rat carotid bodyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0948-6143&volume=130&issue=3&spage=549&epage=559&date=2008&atitle=Chronic+hypoxia+upregulates+the+expression+and+function+of+proinflammatory+cytokines+in+the+rat+carotid+bodyen_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_fulltext-
dc.identifier.doi10.1007/s00418-008-0437-4en_HK
dc.identifier.pmid18446360-
dc.identifier.scopuseid_2-s2.0-50249175017en_HK
dc.identifier.hkuros155514en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-50249175017&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume130en_HK
dc.identifier.issue3en_HK
dc.identifier.spage549en_HK
dc.identifier.epage559en_HK
dc.identifier.isiWOS:000258655300011-
dc.publisher.placeGermanyen_HK
dc.identifier.scopusauthoridLam, SY=7402279518en_HK
dc.identifier.scopusauthoridTipoe, GL=7003550610en_HK
dc.identifier.scopusauthoridLiong, EC=6602732210en_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK
dc.identifier.citeulike3156772-

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