Format

Send to

Choose Destination
J Proteome Res. 2014 Sep 5;13(9):4047-61. doi: 10.1021/pr500431j. Epub 2014 Aug 11.

Chronic sleep deprivation-induced proteome changes in astrocytes of the rat hypothalamus.

Author information

1
Department of Pharmacology, Brain Science & Engineering Institute, BK21 PLUS KNU Biomedical Convergence Program for Creative Talent, ‡Department of Molecular Medicine, Cell & Matrix Research Institute, §Department of Neurology, Brain Science & Engineering Institute, Kyungpook National University School of Medicine , Daegu 700-422, Republic of Korea.

Abstract

Sleep deprivation (SD) can influence cognition, memory, and sleep/wake homeostasis and can cause impairments in many physiological processes. Because the homeostatic control of the sleep/wake cycle is closely associated with the hypothalamus, the current study was undertaken to examine proteomic changes occurring in hypothalamic astrocytes following chronic partial SD. After chronic partial SD for 7 days, astrocytes were prepared from rat hypothalamus using a Percoll gradient method, and their proteome profiles were determined by LC-MS/MS. Comparisons of the proteome profiles of hypothalamic astrocytes revealed that chronic partial SD increased (≥1.5-fold) 89 proteins and decreased (≤0.7-fold) 50 proteins; these changes in protein expression were validated by western blot or immunohistochemistry. DAVID and IPA analyses of these proteins suggested that SD may influence gliotransmission and astrocyte activation. PPP2R1A, RTN4, VAMP-2, LGI-1, and SLC17A7 were identified and validated as the main targets of SD in astrocytes. Our results suggest that SD may modulate gliotransmission in the hypothalamus, thereby disturbing sleep/wake homeostasis and increasing susceptibility to neurological disease; however, further studies are required to confirm whether the proteome changes are specific to SD.

PMID:
25087458
DOI:
10.1021/pr500431j
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for American Chemical Society
Loading ...
Support Center