1-methyl-4-phenylpyridinium ion induces endoplasmic reticulum stress through glycogen synthase kinase-3 beta activation in PC12 cells  

作　　者：Shengdong Wang Fucheng Luo Yan Chen Lei Qi Jie Bai 

机构地区：[1]College of Life Science and Technology, Kunming University of Science and Technology, Kunming 650224, Yunnan Province, China

出　　处：《Neural Regeneration Research》2011年第11期805-810,共6页中国神经再生研究（英文版）

基　　金：the National Natural Science Foundation of China, No. 30860085;a grant from the Candidates of Young and Middle-Aged Academic Leaders of Yunnan Province, No. 2006PY01-07;the Natural Science Foundation of Yunnan Province, No. 2007C177M

摘　　要：1-methyl-4-phenylpyridinium ion （MPP^＋） induces endoplasmic reticulum stress and activates caspase-12 in PC12 cells, leading to neuronal apoptosis. However, the underlying molecular mechanism remains unknown. The present study investigated the regulatory effects of nerve growth factor （Akt activator） and lithium chloride （glycogen synthase kinase-3β inhibitor） on the endoplasmic reticulum stress signaling pathway. The results revealed that MPP＋ induced expression of Bip and C/EBP homologous protein. The upregulation of Bip and C/EBP homologous protein, as well as the decreased pro-caspase-12 level induced by MPP^＋ were inhibited by pretreatment of the nerve growth factor or lithium chloride. These results suggest that the phosphatidylinositol 3 kinase-Aktglycogen synthase kinase-3β pathway is involved in MPP-induced endoplasmic reticulum stress.1-methyl-4-phenylpyridinium ion （MPP^＋） induces endoplasmic reticulum stress and activates caspase-12 in PC12 cells, leading to neuronal apoptosis. However, the underlying molecular mechanism remains unknown. The present study investigated the regulatory effects of nerve growth factor （Akt activator） and lithium chloride （glycogen synthase kinase-3β inhibitor） on the endoplasmic reticulum stress signaling pathway. The results revealed that MPP＋ induced expression of Bip and C/EBP homologous protein. The upregulation of Bip and C/EBP homologous protein, as well as the decreased pro-caspase-12 level induced by MPP^＋ were inhibited by pretreatment of the nerve growth factor or lithium chloride. These results suggest that the phosphatidylinositol 3 kinase-Aktglycogen synthase kinase-3β pathway is involved in MPP-induced endoplasmic reticulum stress.

关 键 词：Parkinson＇s disease 1-methyl-4-phenylpyridinium ion endoplasmic reticulum stress glycogen synthase kinase-3β 

分 类 号：Q78[生物学—分子生物学] Q421