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 language | English |
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Pages (from-to) | 102-112 |
Number of pages | 11 |
Journal | Journal of Neuroimmunology |
Volume | 166 |
Issue number | 1-2 |
DOIs | |
Publication status | Published - Sept 2005 |
Scopus Subject Areas
- Immunology and Allergy
- Immunology
- Neurology
- Clinical Neurology
User-Defined Keywords
- β-adrenergic receptor
- Cell proliferation
- Rat C6 glioma cells
- Tumor necrosis factor-α