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

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.