Caveolin-1 and glucose transporter 4 involved in the regulation of glucose-deprivation stress in PC12 cells.
- Author:
Qi-Qi ZHANG
1
;
Liang HUANG
1
;
Chao HAN
2
;
Xin GUAN
2
;
Ya-Jun WANG
1
;
Jing LIU
2
;
Jing-Hua WAN
3
;
Wei ZOU
1
Author Information
1. College of Life Science, Liaoning Normal University, Dalian 116081, China.
2. Regenerative Medicine Centre, First Affiliated Hospital of Dalian Medical University, Dalian 116011, China.
3. Department of Neurology, the Fifth People's Hospital of Dalian, Dalian 116029, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Calcium;
metabolism;
Caveolin 1;
metabolism;
Gene Knockdown Techniques;
Glucose;
chemistry;
Glucose Transporter Type 4;
metabolism;
Homeostasis;
PC12 Cells;
Protein Transport;
RNA, Small Interfering;
Rats;
Signal Transduction;
Up-Regulation;
beta-Cyclodextrins
- From:
Acta Physiologica Sinica
2015;67(4):349-356
- CountryChina
- Language:English
-
Abstract:
Recent evidence suggests that caveolin-1 (Cav-1), the major protein constituent of caveolae, plays a prominent role in neuronal nutritional availability with cellular fate regulation besides in several cellular processes such as cholesterol homeostasis, regulation of signal transduction, integrin signaling and cell growth. Here, we aimed to investigate the function of Cav-1 and glucose transporter 4 (GLUT4) upon glucose deprivation (GD) in PC12 cells. The results demonstrated firstly that both Cav-1 and GLUT4 were up-regulated by glucose withdrawal in PC12 cells by using Western blot and laser confocal technology. Also, we found that the cell death rate, mitochondrial membrane potential (MMP) and intracellular free Ca(2+) concentration ([Ca(2+)]i) were also respectively changed followed the GD stress tested by CCK8 and flow cytometry. After knocking down of Cav-1 in the cells by siRNA, the level of [Ca(2+)]i was increased, and MMP was reduced further in GD-treated PC12 cells. Knockdown of Cav-1 or methylated-β-Cyclodextrin (M-β-CD) treatment inhibited the expression of GLUT4 protein upon GD. Additionally, we found that GLUT4 could translocate from cytoplasm to cell membrane upon GD. These findings might suggest a neuroprotective role for Cav-1, through coordination of GLUT4 in GD.
