Ischemic preconditioning inhibits over-expression of arginyl-tRNA synthetase gene Rars in ischemia-injured neurons.
10.1007/s11596-016-1624-5
- Author:
Yin SHEN
1
;
Hong-Yang ZHAO
1
;
Hai-Jun WANG
1
;
Wen-Liang WANG
1
;
Li-Zhi ZHANG
1
;
Rong FU
2
Author Information
1. Department of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
2. Department of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. FurongLP@163.com.
- Publication Type:Journal Article
- Keywords:
Rars;
arginyl-tRNA synthetase;
ischemic preconditioning;
oxygen glucose deprivation
- MeSH:
Animals;
Arginine-tRNA Ligase;
biosynthesis;
genetics;
metabolism;
Brain Ischemia;
genetics;
metabolism;
pathology;
Gene Expression Regulation;
genetics;
Glucose;
metabolism;
Humans;
Ischemic Preconditioning;
methods;
Neurons;
metabolism;
pathology;
Oxygen;
metabolism;
Primary Cell Culture;
Rats
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2016;36(4):554-557
- CountryChina
- Language:English
-
Abstract:
The expression changes of Rars gene in ischemia-injured neurons were investigated by detecting its translational product arginyl-tRNA synthetase (ArgRS), and the inhibitory effects of ischemic preconditioning (IPC) on Rars gene were explored. Both IPC model and prolonged ischemia (PI) model were established by using the classic oxygen glucose deprivation (OGD) method. The primary cultured neurons were assigned into the following groups: the experimental group (IPC+PI group), undergoing PI after a short period of IPC; the conditional control group (PI control group), subjected to PI without IPC; blank control group, the normally cultured neurons. The Rars transcriptional activities and ArgRS expression levels were measured at different time points after re-oxygenation (3 h/6 h/12 h/24 h). Data were collected and statistically analyzed. Compared to the blank control group, the Rars activities and ArgRS levels were significantly increased in PI control group, peaking at the time point of 6 h after re-oxygenation. Rars activities and ArgRS levels were significantly lower in the experimental group than in the PI control group at different time points after re-oxygenation. PI insult can induce an escalating activity of Rars and lead to ArgRS over-expression in primary cultured neurons. IPC can inhibit the increased Rars activity and down-regulate ArgRS expression of ischemia-insulted neurons. This mechanism may confer ischemic tolerance on neurons.
