Lung Hong-Lok, Shan Sze-Wan, Tsang David, Leung Kwok-Nam
Department of Biochemistry, The Chinese University of Hong Kong, Shatin, Hong Kong, China.
J Neuroimmunol. 2005 Sep;166(1-2):102-12. doi: 10.1016/j.jneuroim.2005.05.011.
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.
在本研究中，我们观察到β-肾上腺素能受体（β-AR）激动剂异丙肾上腺素可刺激大鼠C6胶质瘤细胞增殖，而β-AR阻滞剂普萘洛尔则大大降低了TNF-α对C6细胞的增殖作用。TNF-α处理后，C6细胞中β1-AR和β2-AR的基因及蛋白表达均增强，β-AR的增加是由于结合位点数量增加，而非受体亲和力增加。我们进一步表明蛋白激酶C（PKC）参与了TNF-α诱导的β-AR表达。总体而言，我们的结果表明，TNF-α诱导的C6胶质瘤细胞增殖可能是通过β-AR的诱导和激活实现的。
