Decreased GLT-1 and increased SOD1 and HO-1 expression in astrocytes contribute to lumbar spinal cord vulnerability of SOD1-G93A transgenic mice

被引:24
作者
Guo, Yansu [1 ,2 ,3 ]
Duan, Weisong [1 ,2 ,3 ]
Li, Zhongyao [1 ,2 ,3 ]
Huang, Jing [1 ,2 ,3 ]
Yin, Yunxia [1 ]
Zhang, Kunxi [1 ]
Wang, Qian [1 ]
Zhang, Zhifang [1 ]
Li, Chunyan [1 ,2 ,3 ]
机构
[1] Hebei Med Univ, Hosp 2, Dept Neurol, Shijiazhuang, Hebei Province, Peoples R China
[2] Hebei Med Univ, Hosp 2, Hebei Prov Key Lab Neurol, Shijiazhuang, Hebei Province, Peoples R China
[3] Inst Cardiocerebrovasc, Shijiazhuang, Hebei, Peoples R China
来源
FEBS LETTERS | 2010年 / 584卷 / 08期
关键词
ALS; Astrocyte; SOD1; Heme oxygenase-1; Transgenic mice; AMYOTROPHIC-LATERAL-SCLEROSIS; GLIAL GLUTAMATE TRANSPORTER; HEME OXYGENASE-1; ENDOTHELIAL-CELLS; DISEASE ONSET; MODEL; ALS; PROGRESSION; SUPEROXIDE; INJURY;
D O I
10.1016/j.febslet.2010.03.025
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The SOD1-G93A transgenic mouse is a widely used ALS model, but the death of lower motor neurons is the hallmark. Here, we show that the SOD1-G93A transgene and HO-1 are preferentially over-expressed in the lumbar spinal cord, particularly in the activated astrocytes of the transgenic mice. We also show down-regulation of GLT-1 in spite of the proliferating astrocytes. However, GLT-1, SOD1-G93A transgene and HO-1 expression were not obviously changed in the motor cortex. Our data link spinal cord vulnerability to relatively decreased expression of GLT-1, and high expression of the transgene and HO-1 in astrocytes in SOD1-G93A transgenic mice. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
引用
收藏
页码:1615 / 1622
页数:8
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