Interleukin-6 protects cultured cerebellar granule neurons against glutamate-induced neurotoxicity. Export

@article{Peng2005, abstract = {Cytokine interleukin-6 (IL-6) has been showed to be an important mediator of neuroimmune responses. However, effects of IL-6 in the central nervous system (CNS) are quite complex and diverse, and mechanisms through which IL-6 influences neuronal functions are primarily unknown. In the present study, we explored protective effect of IL-6 that was chronically applied to cerebellar granule neurons (CGNs) in culture against neurodamage induced by glutamate and mechanisms involved in the neuroprotective effect of IL-6. The chronic IL-6 exposure significantly prevented the CGNs from the glutamate-induced attenuation of neuronal vitality. This neuroprotective effect of IL-6 depended on its concentrations. IL-6 at 2.5 ng/ml did not markedly improve the neuronal vitality, but IL-6 at 5 and 10 ng/ml notably improved the neuronal vitality. The glutamate-evoked neuronal apoptosis also was strikingly inhibited by the chronic IL-6 pretreatment. Intracellular Ca2+ in the CGNs lacking IL-6 pretreatment acutely rose as soon as these neurons were stimulated by glutamate and were maintained at higher levels during the whole 18-min period of glutamate attack. Although intracellular Ca2+ in the IL-6-pretreated CGNs also produced an acute and transient elevation in response to the glutamate insult, they quickly dropped and recovered to basal levels before the glutamate application. Anti-gp130 monoclonal antibody (mAb) blocked the suppressive effect of IL-6 on the glutamate-induced intracellular Ca2+ overload. These results reveal that IL-6 can protect neurons against glutamate-induced neurotoxicity, and suggest that the neuroprotective effect of IL-6 may be via gp130 signal transducing pathway to suppress the glutamate-evoked intracellular Ca2+ overload.}, address = {Department of Biological Science and Technology and State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Mailbox 426, Nanjing University, 22 Hankou Road, Nanjing 210093, China.}, author = {Peng, Y. P. and Qiu, Y. H. and Lu, J. H. and Wang, J. J.}, citeulike-article-id = {883541}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/j.neulet.2004.10.069}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/15663961}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=15663961}, citeulike-linkout-3 = {http://www.sciencedirect.com/science/article/B6T0G-4DW98XP-2/2/c3c65bb09daddaca4c010e25223ef0c9}, day = {21}, doi = {10.1016/j.neulet.2004.10.069}, issn = {0304-3940}, journal = {Neurosci Lett}, keywords = {effects, function, il6}, month = {February}, number = {3}, pages = {192--196}, posted-at = {2006-10-04 09:35:05}, priority = {2}, title = {Interleukin-6 protects cultured cerebellar granule neurons against glutamate-induced neurotoxicity.}, url = {http://dx.doi.org/10.1016/j.neulet.2004.10.069}, volume = {374}, year = {2005} }

TY - JOUR ID - Peng2005 L3 - citeulike-article-id:883541 N2 - Cytokine interleukin-6 (IL-6) has been showed to be an important mediator of neuroimmune responses. However, effects of IL-6 in the central nervous system (CNS) are quite complex and diverse, and mechanisms through which IL-6 influences neuronal functions are primarily unknown. In the present study, we explored protective effect of IL-6 that was chronically applied to cerebellar granule neurons (CGNs) in culture against neurodamage induced by glutamate and mechanisms involved in the neuroprotective effect of IL-6. The chronic IL-6 exposure significantly prevented the CGNs from the glutamate-induced attenuation of neuronal vitality. This neuroprotective effect of IL-6 depended on its concentrations. IL-6 at 2.5 ng/ml did not markedly improve the neuronal vitality, but IL-6 at 5 and 10 ng/ml notably improved the neuronal vitality. The glutamate-evoked neuronal apoptosis also was strikingly inhibited by the chronic IL-6 pretreatment. Intracellular Ca2+ in the CGNs lacking IL-6 pretreatment acutely rose as soon as these neurons were stimulated by glutamate and were maintained at higher levels during the whole 18-min period of glutamate attack. Although intracellular Ca2+ in the IL-6-pretreated CGNs also produced an acute and transient elevation in response to the glutamate insult, they quickly dropped and recovered to basal levels before the glutamate application. Anti-gp130 monoclonal antibody (mAb) blocked the suppressive effect of IL-6 on the glutamate-induced intracellular Ca2+ overload. These results reveal that IL-6 can protect neurons against glutamate-induced neurotoxicity, and suggest that the neuroprotective effect of IL-6 may be via gp130 signal transducing pathway to suppress the glutamate-evoked intracellular Ca2+ overload. IS - 3 JF - Neurosci Lett SN - 0304-3940 AD - Department of Biological Science and Technology and State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Mailbox 426, Nanjing University, 22 Hankou Road, Nanjing 210093, China. EP - 196 TI - Interleukin-6 protects cultured cerebellar granule neurons against glutamate-induced neurotoxicity. VL - 374 SP - 192 KW - effects KW - function KW - il6 AU - Peng, YP AU - Qiu, YH AU - Lu, JH AU - Wang, JJ PY - 2005/02/21/ UR - http://dx.doi.org/10.1016/j.neulet.2004.10.069 ER -