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Decreased GLT‐1 and increased SOD1 and HO‐1 expression in astrocytes contribute to lumbar spinal cord vulnerability of SOD1‐G93A transgenic mice
Author(s) -
Guo Yansu,
Duan Weisong,
Li Zhongyao,
Huang Jing,
Yin Yunxia,
Zhang Kunxi,
Wang Qian,
Zhang Zhifang,
Li Chunyan
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.03.025
Subject(s) - transgene , sod1 , spinal cord , genetically modified mouse , lumbar spinal cord , astrocyte , biology , microbiology and biotechnology , spinal cord injury , neuroscience , central nervous system , endocrinology , gene , oxidative stress , genetics , superoxide dismutase
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.