Relationship between ER-α36 and Akt in PC12 cells exposed to glucose deprivation.
- Author:
Xiao-Feng LIANG
1
,
2
,
3
;
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
2. The Research Center of Developmental and Educational Psychology, Liaoning Normal University, Dalian 116029, China
3. Regenerative Medicine Centre, First Affiliated Hospital of Dalian Medical University, Dalian 116011, China. E-mail: weizou60@126.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.
