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首页> 外文期刊>The European Journal of Neuroscience >Peripheral but not central axotomy induces changes in Janus kinases (JAK) and signal transducers and activators of transcription (STAT).
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Peripheral but not central axotomy induces changes in Janus kinases (JAK) and signal transducers and activators of transcription (STAT).

机译：外围而非中心轴切术可引起Janus激酶（JAK）以及信号转导和转录激活因子（STAT）的变化。

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摘要

Nerve injury leads to the release of a number of cytokines which have been shown to play an important role in cellular activation after peripheral nerve injury. The members of the signal transducer and activator of transcription (STAT) gene family are the main mediators in the signal transduction pathway of cytokines. After phosphorylation, STAT proteins are transported into the nucleus and exhibit transcriptional activity. Following axotomy in rat regenerating facial and hypoglossal neurons, a transient increase of mRNA for JAK2, JAK3, STAT1, STAT3 and STAT5 was detected using in situ hybridization and semi-quantitative polymerase chain reaction (PCR). Of the investigated STAT molecules, only STAT3 protein was significantly increased. In addition, activation of STAT3 by phosphorylation on position Tyr705 and enhanced nuclear translocation was found within 3 h in neurons and after 1 day in astrocytes. Unexpectedly, STAT3 tyrosine phosphorylation was obvious for more than 3 months. In contrast, none of these changes was found in response to axotomy of non-regenerating Clarke's nucleus neurons, although all the investigated models express c-Jun and growth-associated protein-43 (GAP-43) in response to axonal injury. Increased expression of Janus kinase (JAK) and STAT molecules after peripheral nerve transection suggests changes in the responsiveness of the neurons to signalling molecules. STAT3 as a transcription factor, which is expressed early and is activated persistently until the time of reinnervation, might be involved in the switch from the physiological gene expression to an 'alternative program' activated only after peripheral nerve injury.
机译：神经损伤导致许多细胞因子的释放，这些细胞因子已被证明在周围神经损伤后在细胞活化中起重要作用。信号转导子和转录激活子（STAT）基因家族的成员是细胞因子信号转导途径中的主要介体。磷酸化后，STAT蛋白被转运到细胞核中并表现出转录活性。在大鼠再生的面部和舌下神经元神经切断后，使用原位杂交和半定量聚合酶链反应（PCR）检测到JAK2，JAK3，STAT1，STAT3和STAT5 mRNA的瞬时增加。在研究的S​​TAT分子中，仅STAT3蛋白显着增加。此外，在神经元的3小时内和星形胶质细胞的1天后，发现Tyr705位置的磷酸化激活STAT3和增强的核易位。出乎意料的是，STAT3酪氨酸磷酸化明显超过3个月。相反，尽管所有研究的模型均响应轴突损伤而表达c-Jun和生长相关蛋白43（GAP-43），但这些变化均未响应非再生克拉克核神经元的轴切术而被发现。周围神经横断后，Janus激酶（JAK）和STAT分子的表达增加表明神经元对信号分子的反应性发生了变化。 STAT3作为一种转录因子，在早期表达并持续被激活直至重新神经支配，可能参与了从生理基因表达到仅在周围神经损伤后激活的“替代程序”的转换。

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