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Article: Tumor necrosis factor-α mediates the proliferation of rat C6 glioma cells via β-adrenergic receptors

TitleTumor necrosis factor-α mediates the proliferation of rat C6 glioma cells via β-adrenergic receptors
Authors
Issue Date2005
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/jneuroim
Citation
Journal Of Neuroimmunology, 2005, v. 166 n. 1-2, p. 102-112 How to Cite?
AbstractIn the present study, we observed that isoproterenol, a β-adrenergic receptor (β-AR) agonist, stimulated rat C6 glioma cell proliferation, while propranolol, a β-AR blocker, greatly reduced the proliferative effect of TNF-α on C6 cells. The gene and protein expressions of both β1- and β2-ARs were enhanced in C6 cells after TNF-α treatment, and the increase in β-AR was due to an increased number of binding sites and not due to increase in receptor affinity. We further showed that protein kinase C (PKC) was involved in the TNF-α-induced β-AR expression. Collectively, our results indicate that TNF-α-induced proliferation in C6 glioma cells might be via the induction and activation of β-ARs. © 2005 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/150794
ISSN
2015 Impact Factor: 2.536
2015 SCImago Journal Rankings: 1.165
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLung, HLen_US
dc.contributor.authorShan, SWen_US
dc.contributor.authorTsang, Den_US
dc.contributor.authorLeung, KNen_US
dc.date.accessioned2012-06-26T06:10:36Z-
dc.date.available2012-06-26T06:10:36Z-
dc.date.issued2005en_US
dc.identifier.citationJournal Of Neuroimmunology, 2005, v. 166 n. 1-2, p. 102-112en_US
dc.identifier.issn0165-5728en_US
dc.identifier.urihttp://hdl.handle.net/10722/150794-
dc.description.abstractIn the present study, we observed that isoproterenol, a β-adrenergic receptor (β-AR) agonist, stimulated rat C6 glioma cell proliferation, while propranolol, a β-AR blocker, greatly reduced the proliferative effect of TNF-α on C6 cells. The gene and protein expressions of both β1- and β2-ARs were enhanced in C6 cells after TNF-α treatment, and the increase in β-AR was due to an increased number of binding sites and not due to increase in receptor affinity. We further showed that protein kinase C (PKC) was involved in the TNF-α-induced β-AR expression. Collectively, our results indicate that TNF-α-induced proliferation in C6 glioma cells might be via the induction and activation of β-ARs. © 2005 Elsevier B.V. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/jneuroimen_US
dc.relation.ispartofJournal of Neuroimmunologyen_US
dc.subject.meshAdrenergic Beta-Antagonists - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCell Proliferation - Drug Effectsen_US
dc.subject.meshDihydroalprenolol - Metabolismen_US
dc.subject.meshGlioma - Metabolism - Pathologyen_US
dc.subject.meshProtein Kinase C - Physiologyen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshReceptors, Adrenergic, Beta-1 - Genetics - Metabolism - Physiologyen_US
dc.subject.meshReceptors, Adrenergic, Beta-2 - Genetics - Metabolism - Physiologyen_US
dc.subject.meshTumor Necrosis Factor-Alpha - Pharmacologyen_US
dc.titleTumor necrosis factor-α mediates the proliferation of rat C6 glioma cells via β-adrenergic receptorsen_US
dc.typeArticleen_US
dc.identifier.emailLung, HL:hllung2@hku.hken_US
dc.identifier.authorityLung, HL=rp00299en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.jneuroim.2005.05.011en_US
dc.identifier.pmid16005083-
dc.identifier.scopuseid_2-s2.0-23044468794en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-23044468794&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume166en_US
dc.identifier.issue1-2en_US
dc.identifier.spage102en_US
dc.identifier.epage112en_US
dc.identifier.isiWOS:000231487100011-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridLung, HL=6603819904en_US
dc.identifier.scopusauthoridShan, SW=8509293300en_US
dc.identifier.scopusauthoridTsang, D=7005609135en_US
dc.identifier.scopusauthoridLeung, KN=7401860476en_US

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