title: Tumor necrosis factor-alpha mediates the proliferation of rat C6 glioma cells via beta-adrenergic receptors.
abstract: In the present study, we observed that isoproterenol, a beta-adrenergic receptor (beta-AR) agonist, stimulated rat C6 glioma cell proliferation, while propranolol, a beta-AR blocker, greatly reduced the proliferative effect of TNF-alpha on C6 cells. The gene and protein expressions of both beta1- and beta2-ARs were enhanced in C6 cells after TNF-alpha treatment, and the increase in beta-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-alpha-induced beta-AR expression. Collectively, our results indicate that TNF-alpha-induced proliferation in C6 glioma cells might be via the induction and activation of beta-ARs.
authors: Department of Biochemistry, The Chinese University of Hong Kong, Shatin, Hong Kong, China.
authors: Hong-Lok
authors: HL
authors: Lung
authors: Sze-Wan
authors: SW
authors: Shan
authors: David
authors: D
authors: Tsang
authors: Kwok-Nam
authors: KN
authors: Leung
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000378:metabolism; D000818:Animals; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D004082:Dihydroalprenolol / Q000378:metabolism; D005910:Glioma / Q000378:metabolism* / Q000473:pathology*; D011493:Protein Kinase C / Q000502:physiology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D018342:Receptors, Adrenergic, beta-1 / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D018343:Receptors, Adrenergic, beta-2 / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
chemical_list: D000319:Adrenergic beta-Antagonists; D012333:RNA, Messenger; D018342:Receptors, Adrenergic, beta-1; D018343:Receptors, Adrenergic, beta-2; D014409:Tumor Necrosis Factor-alpha; D004082:Dihydroalprenolol; D011493:Protein Kinase C