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

Hong Lok Lung, Sze Wan Shan, David Tsang, Kwok Nam Leung

Research output: Journal article publicationJournal articleAcademic researchpeer-review

15 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)102-112
Number of pages11
JournalJournal of Neuroimmunology
Volume166
Issue number1-2
DOIs
Publication statusPublished - Sep 2005
Externally publishedYes

Keywords

  • β-adrenergic receptor
  • Cell proliferation
  • Rat C6 glioma cells
  • Tumor necrosis factor-α

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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