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- Publisher Website: 10.1016/j.jneuroim.2005.05.011
- Scopus: eid_2-s2.0-23044468794
- PMID: 16005083
- WOS: WOS:000231487100011
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Article: Tumor necrosis factor-α mediates the proliferation of rat C6 glioma cells via β-adrenergic receptors
Title | Tumor necrosis factor-α mediates the proliferation of rat C6 glioma cells via β-adrenergic receptors |
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Authors | |
Keywords | β-adrenergic receptor Cell proliferation Rat C6 glioma cells Tumor necrosis factor-α |
Issue Date | 2005 |
Publisher | Elsevier 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? |
Abstract | In 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 Identifier | http://hdl.handle.net/10722/150794 |
ISSN | 2023 Impact Factor: 2.9 2023 SCImago Journal Rankings: 0.897 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lung, HL | en_US |
dc.contributor.author | Shan, SW | en_US |
dc.contributor.author | Tsang, D | en_US |
dc.contributor.author | Leung, KN | en_US |
dc.date.accessioned | 2012-06-26T06:10:36Z | - |
dc.date.available | 2012-06-26T06:10:36Z | - |
dc.date.issued | 2005 | en_US |
dc.identifier.citation | Journal Of Neuroimmunology, 2005, v. 166 n. 1-2, p. 102-112 | en_US |
dc.identifier.issn | 0165-5728 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/150794 | - |
dc.description.abstract | In 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.language | eng | en_US |
dc.publisher | Elsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/jneuroim | en_US |
dc.relation.ispartof | Journal of Neuroimmunology | en_US |
dc.subject | β-adrenergic receptor | - |
dc.subject | Cell proliferation | - |
dc.subject | Rat C6 glioma cells | - |
dc.subject | Tumor necrosis factor-α | - |
dc.subject.mesh | Adrenergic Beta-Antagonists - Metabolism | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Cell Line, Tumor | en_US |
dc.subject.mesh | Cell Proliferation - Drug Effects | en_US |
dc.subject.mesh | Dihydroalprenolol - Metabolism | en_US |
dc.subject.mesh | Glioma - Metabolism - Pathology | en_US |
dc.subject.mesh | Protein Kinase C - Physiology | en_US |
dc.subject.mesh | Rna, Messenger - Metabolism | en_US |
dc.subject.mesh | Rats | en_US |
dc.subject.mesh | Receptors, Adrenergic, Beta-1 - Genetics - Metabolism - Physiology | en_US |
dc.subject.mesh | Receptors, Adrenergic, Beta-2 - Genetics - Metabolism - Physiology | en_US |
dc.subject.mesh | Tumor Necrosis Factor-Alpha - Pharmacology | en_US |
dc.title | Tumor necrosis factor-α mediates the proliferation of rat C6 glioma cells via β-adrenergic receptors | en_US |
dc.type | Article | en_US |
dc.identifier.email | Lung, HL:hllung2@hku.hk | en_US |
dc.identifier.authority | Lung, HL=rp00299 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1016/j.jneuroim.2005.05.011 | en_US |
dc.identifier.pmid | 16005083 | - |
dc.identifier.scopus | eid_2-s2.0-23044468794 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-23044468794&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 166 | en_US |
dc.identifier.issue | 1-2 | en_US |
dc.identifier.spage | 102 | en_US |
dc.identifier.epage | 112 | en_US |
dc.identifier.isi | WOS:000231487100011 | - |
dc.publisher.place | Netherlands | en_US |
dc.identifier.scopusauthorid | Lung, HL=6603819904 | en_US |
dc.identifier.scopusauthorid | Shan, SW=8509293300 | en_US |
dc.identifier.scopusauthorid | Tsang, D=7005609135 | en_US |
dc.identifier.scopusauthorid | Leung, KN=7401860476 | en_US |
dc.identifier.issnl | 0165-5728 | - |