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首页> 外文期刊>The European Journal of Neuroscience >Differential activation of neuronal and glial STAT3 in the spinal cord of the SOD1(G93A) mouse model of amyotrophic lateral sclerosis
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Differential activation of neuronal and glial STAT3 in the spinal cord of the SOD1(G93A) mouse model of amyotrophic lateral sclerosis

机译：肌营养横向硬化脊髓脊髓脊髓神经元和神经胶凝STAT3的差异激活

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Signal transducer and activator of transcription (STAT) proteins are activated by phosphorylation in the spinal cord of patients suffering from amyotrophic lateral sclerosis (ALS). The major scope of our study is a comprehensive histological characterization of the mechanisms underlying neuronal and glial STAT3 activation in the pathogenesis of ALS using SOD1(G93A) mice. We calculated the fold changes (FCs, ratios vs. appropriate controls) of the numerical densities of the following phosphorylated STAT3-positive (pSTAT3)(+) cells - choline acetyltransferase (ChAT)(+) -motoneurons, ionized calcium-binding adapter molecule 1 (Iba1)(+) microglia, and S100(+) astrocytes in SOD1(G93A) mice. The FCs of pSTAT3(+) microglia and pSTAT3(+) astrocytes were increased from 9 to 15weeks of age and then plateaued until 21weeks. In contrast, the FCs of pSTAT3(+) -motoneurons peaked at 9weeks and then decreased until 21weeks. The immunoreactivity for nonphosphorylated neurofilament protein (SMI-32), a marker of axonal impairment, was decreased in pSTAT3(+) -motoneurons compared with pSTAT3(-) -motoneurons at 9weeks of age. We then compared the following pharmacological models - the chronic administration of 3,3-iminodipropionitrile (IDPN), which models axonal impairment, and the acute administration of lipopolysaccharide (LPS), which is a model of neuroinflammation. The FCs of pSTAT3(+) -motoneurons were increased in IDPN-treated mice, while those of pSTAT3(+) microglia were increased in LPS-treated mice. The FCs of pSTAT3(+) astrocytes were higher in SOD1(G93A) mice at 9weeks compared with IDPN- and LPS-treated mice. Our results indicate that axonopathy and neuroinflammation may trigger the respective activation of neuronal and glial STAT3, which is observed during ALS pathogenesis.
机译：通过患肌萎缩横向硬化（ALS）的患者的脊髓中磷酸化激活转录（统计）蛋白的信号传感器和活化剂。我们研究的主要范围是使用SOD1（G93A）小鼠在ALS发病机制中神经元和神经胶凝毒率3激活的机制的综合组织学表征。我们计算了以下磷酸化的STAT3阳性（PSTAT3）（+）细胞 - 胆碱乙酰转移酶（聊天）（+）-Motoneurons，电离钙结合衔接子分子的数值密度的折叠变化（FCS，比率与适当对照）的数值密度1（IBA1）（+）微胶质细胞和SOD1（G93A）小鼠的S100（+）星形胶质细胞。 PSTAT3（+）微胶质细胞和PSTAT3（+）星形胶质细胞的FCS从9至15周的年龄增加，然后达到平稳，直到21周。相比之下，Pstat3（+）-Motoneurons的Fcs在9周上达到峰值，然后减少到21周。与Pstat3（ - ）-Motoneurons相比，非磷酸化神经丝蛋白（SMI-32），轴突损伤标志物，轴突损伤标志物，与Pstat3（ - ）-Motoneurons在年龄为9周。然后比较以下药理学模型 - 慢性施用3,3-亚单哌洛哌洛可（IDPN），其模型轴突损伤，以及脂多糖（LPS）的急性施用，这是神经引发的模型。在IDPN处理的小鼠中增加了Pstat3（+）-Motoneurons的Fcs，而Pstat3（+）微胶质细胞的小鼠的FC在LPS处理的小鼠中增加。与IDPN和LPS处理的小鼠相比，9周的SOD1（G93A）小鼠的PSTAT3（+）星形胶质细胞的FC在9周内较高。我们的结果表明，腋病和神经炎性炎症可以触发在ALS发病机制期间观察到的神经元和神经胶质局的各自的激活。

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