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Spatio-temporal expression of Hexokinase-3 in the injured female rat spinal cords.

Authors :
Lin, Yu-Hong
Wu, Yan
Wang, Ying
Yao, Zong-Feng
Tang, Jie
Wang, Rui
Shen, Lin
Ding, Shu-Qin
Hu, Jian-Guo
Lü, He-Zuo
Source :
Neurochemistry International. Feb2018, Vol. 113, p23-33. 11p.
Publication Year :
2018

Abstract

Hexokinase-3 (HK3) is a member of hexokinase family, which can catalyze the first step of glucose metabolism. It can increase ATP levels, reduce the production of reactive oxygen species, increase mitochondrial biogenesis, protect mitochondrial membrane potential and play an antioxidant role. However, the change of its expression in spinal cord after injury is still unknown. In this study, we investigated the spatio-temporal expression of HK3 in the spinal cords by using a spinal cord injury (SCI) model in adult female Sprague-Dawley rats. Quantitative reverse transcription-PCR and western blot analysis revealed that HK3 could be detected in sham-opened spinal cords. After SCI, it gradually increased, reached a peak at 7 days post-injury (dpi), and then gradually decreased with the prolonging of injury time, but still maintained at a higher level for up to 28 dpi (the longest time evaluated in this study). Immunofluorescence staining showed that HK3 was found in GFAP + , β-tubulin III + and IBA-1 + cells in sham-opened spinal cords. After SCI, in addition to the above-mentioned cells, it could also be found in CD45 + and CD68 + cells. These results demonstrate that HK3 is mainly expressed in astrocytes, neurons and microglia in normal spinal cords, and could rapidly increase in infiltrated leukocytes, activated microglia/macrophages and astrocytes after SCI. These data suggest that HK3 may be involved in the pathologic process of SCI by promoting glucose metabolism. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
01970186
Volume :
113
Database :
Academic Search Index
Journal :
Neurochemistry International
Publication Type :
Academic Journal
Accession number :
128166583
Full Text :
https://doi.org/10.1016/j.neuint.2017.11.015