title: [Relationship between ER-α36 and Akt in PC12 cells exposed to glucose deprivation].
abstract: ER-α36 is a novel 36-kDa variant of ER-α. A large of evidence demonstrated that ER-α36 responded to membrane-initiated estrogen signaling pathways which were involved in the physiological and pathological process in many kinds of cells. In this study, knock-down of ER-α36 expression in pheochromocytoma (PC12) cells (named as PC12-36L cells) by using the shRNA method was used to evaluate the relationship between ER-α36 and Akt in neurons under glucose deprivation. The effect of ER-α36 on outgrowth of PC12 cells, as well as the neuroprotective effect of ER-α36 on injured PC12 cells exposed to glucose deprivation was observed by using MTT assay, Western blot and Annexin V/PI staining et al. The results showed that, (1) Glucose deprivation induced by MEM treatment for 6 h reduced survival rate and increased apoptotic rate in PC12 cells significantly compared to control group (P < 0.01); and it produced a decrease in the expression of Glut-4 protein (P < 0.01); (2) The expression level of ER-α36 was decreased significantly at 3 h of glucose deprivation, and then increased, while phosphorylation of Akt participated in the glucose deprivation was increased at first and then reduced; LY294002 (PI3K inhibitor) contributed to decreased expression of ER-α36, and suppressed the activation of Akt; (3) The rate of apoptosis was significantly increased in PC12-36L cells after glucose deprivation compared with that in wild type PC12 cells (P < 0.01). Furthermore, phosphorylation of Akt was decreased and Caspase-3 was increased by glucose deprivation in PC12-36L cells compared with those in wild type PC12 cells. The study reveals that phosphorylation of Akt is associated with ER-α36 in PC12 cells exposed to glucose deprivation, and both are involved in the regulation of stress responses.
authors: College of Life Science, Liaoning Normal University, Dalian 116021, China; The Research Center of Developmental and Educational Psychology, Liaoning Normal University, Dalian 116029, China; Regenerative Medicine Centre, First Affiliated Hospital of Dalian Medical University, Dalian 116011, China. E-mail: weizou60@126.com.
authors: Xiao-Feng
authors: XF
authors: Liang
authors: Chen
authors: C
authors: Fang
authors: Yi-Ni
authors: YN
authors: Ma
authors: Xin
authors: X
authors: Guan
authors: Yang
authors: Y
authors: Liu
authors: Chao
authors: C
authors: Han
authors: Jing
authors: J
authors: Liu
authors: Wei
authors: W
authors: Zou
mesh_terms: D000818:Animals; D017209:Apoptosis; D053148:Caspase 3 / Q000378:metabolism; D002867:Chromones / Q000494:pharmacology; D003470:Culture Media / Q000737:chemistry; D047628:Estrogen Receptor alpha / Q000378:metabolism*; D005947:Glucose / Q000737:chemistry; D009025:Morpholines / Q000494:pharmacology; D016716:PC12 Cells; D000081082:Phosphoinositide-3 Kinase Inhibitors; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D051381:Rats; D015398:Signal Transduction
chemical_list: D002867:Chromones; D003470:Culture Media; D047628:Estrogen Receptor alpha; D009025:Morpholines; D000081082:Phosphoinositide-3 Kinase Inhibitors; C085911:2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; D051057:Proto-Oncogene Proteins c-akt; C505410:Casp3 protein, rat; D053148:Caspase 3; D005947:Glucose