Relationship between ER-α36 and Akt in PC12 cells exposed to glucose deprivation.
- Author:
Xiao-Feng LIANG
1
,
2
;
Chen FANG
;
Yi-Ni MA
;
Xin GUAN
;
Yang LIU
;
Chao HAN
;
Jing LIU
;
Wei ZOU
Author Information
1. 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@
2. com.
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
Caspase 3;
metabolism;
Chromones;
pharmacology;
Culture Media;
chemistry;
Estrogen Receptor alpha;
metabolism;
Glucose;
chemistry;
Morpholines;
pharmacology;
PC12 Cells;
Phosphatidylinositol 3-Kinases;
antagonists & inhibitors;
Phosphorylation;
Proto-Oncogene Proteins c-akt;
metabolism;
Rats;
Signal Transduction
- From:
Acta Physiologica Sinica
2013;65(4):381-388
- CountryChina
- Language:Chinese
-
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.
