首页> 外文期刊>FEBS letters. >Decreased GLT-1 and increased SOD1 and HO-1 expression in astrocytes contribute to lumbar spinal cord vulnerability of SOD1-G93A transgenic mice.
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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.

机译:星形胶质细胞中GLT-1的减少以及SOD1和HO-1的表达增加,导致了SOD1-G93A转基因小鼠的腰脊髓易损性。

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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.
机译:SOD1-G93A转基因小鼠是一种广泛使用的ALS模型,但下运动神经元的死亡是标志。在这里,我们显示SOD1-G93A转基因和HO-1优先在腰脊髓中过表达,特别是在转基因小鼠的活化星形胶质细胞中过表达。尽管星形胶质细胞增生,我们也显示出GLT-1的下调。然而,运动皮层中GLT-1,SOD1-G93A转基因和HO-1的表达没有明显改变。我们的数据将脊髓脆弱性联系到SOD1-G93A转基因小鼠星形胶质细胞中GLT-1相对降低的表达以及转基因和HO-1的高表达。

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