@inproceedings{oai:kansai-u.repo.nii.ac.jp:00003134,
 author = {池内, 俊彦 and Ikeuchi, Toshihiko and 下家, 浩二},
 book = {第11回関西大学先端科学技術シンポジウム講演集},
 month = {Jan},
 note = {Neuronal degenerative diseases including Alzheimer's, Parkinson's and polyglutamine diseases are considered to involve endoplasmic reticulum (ER) stress, which leads to ER stress-mediated apoptosis of some neurons. In the process of these diseases, it has been reported that unfolded proteins are accumulated in the ER and this step is critical for progression of neuronal apoptosis through the caspase cascade involving an ER stress-specific caspase, caspase-12. During ER stress, chaperone proteins including glucose-regulated protein 78 (GRP78) are expressed to fold these unfolded proteins as an unfolded protein response (UPR). In cultured cells, ER stress can be induced by tunicamycin (Tm) or thapsigargin (Tg). 
We report that nerve growth factor (NGF), a well-known member of the neurotrophin family, suppressed Tm-, Tg- and 2-deoxy-glucose (2DG)-induced ER stress-mediated apoptosis in PC12 cells as a model neuron. NGF prevented the progression of ER stress-induced apoptosis by the suppression of activation of caspase-12 via the PI3-kinase-Akt signaling pathway. NGF up-regulated the ER stress-stimulated expression of GRP78, but this up-regulation of GRP78 by NGF did not contribute to the protective effect ofNGF on ER stress-induced apoptosis. 
We found that nicotine protected against Tm-induced ER stress-mediated apoptosis but not Tg-induced ER stress-mediated apoptosis in PC12 cells. We also found that the expression of GRP78 was suppressed by nicotine in Tm-treated PC12 cells. Interestingly, the expression of GRP78 was not changed by nicotine in Tg-treated cells. Moreover, nicotine reduced the activation of caspase-12 in Tm-treated cells, but not in Tg-treated cells. These results suggest that nicotine prevents Tm-induced ER stress-mediated apoptosis by attenuating Tm-induced ER stress itself, probably by the clearance of accumulated unfolded proteins from the ER., This work was supported in part by grants-in-aid for scientific research from MEXT, HAITEKU (2002-2006) from MEXT and a research grant from the Smoking Research Foundation.},
 pages = {109--116},
 publisher = {関西大学先端科学技術推進機構},
 title = {神経系小胞体ストレスと誘導型アポトーシスのニコチンとニューロトロフィンによる防御機構},
 year = {2007}
}