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首页> 外文期刊>The European Journal of Neuroscience >The role of MAP kinases in rapid gene induction after lesioning of the rat sciatic nerve.
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The role of MAP kinases in rapid gene induction after lesioning of the rat sciatic nerve.

机译：MAP激酶在大鼠坐骨神经损伤后快速基因诱导中的作用。

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Abstract Lesion of the sciatic nerve caused a rapid activation of p38MAP kinase in the injured nerve adjacent to the site of transection. This activation was detectable 3 min after lesioning, increased during the next 15 min and remained high for several hours. Erk1/2 activation was also observed as early as 15 min after lesioning. Activation of these MAP kinases was seen in both the external sheaths and the endoneurium. The separation of the external sheaths from the endoneurium accelerated the p38MAP kinase activation. To evaluate whether the injury-activated MAP kinase cascades are implicated in the rapid gene induction observed after nerve lesion, experiments were performed with an ex vivo model. Segments of sciatic nerves were incubated in oxygenated Krebs-Ringer buffer. MAP kinases were activated at 15 min and remained active after 6 h. Induction of mRNA was also observed for nerve growth factor (NGF), interleukin 6 (IL-6), leukaemia inhibitory factor (LIF) and deiodinases of type 2 (D2) and type3 (D3). Thus, the ex vivo model mimics events occurring in the animal after nerve section. Finally, nerve segments were incubated in the presence of specific inhibitors of Erk1/2 activation (U0126) and of p38MAP kinase activity (SB203580). U0126 inhibited D3, LIF and to a lesser extent NGF mRNA induction, but did not affect significantly the induction of D2 and IL-6 mRNAs. SB203580 inhibited the expression of the genes for D3 and LIF. We conclude that MAP kinase cascades, activated by nerve transection, are involved in the rapid gene induction in the nerve.
机译：摘要坐骨神经损伤导致邻近横断部位的受伤神经中p38MAP激酶快速激活。损伤后3分钟可检测到该激活，在接下来的15分钟内增加，并持续数小时。早在病变后15分钟也观察到Erk1 / 2激活。在外部鞘和神经内膜中均可见到这些MAP激酶的活化。外鞘与神经内膜的分离加速了p38MAP激酶的活化。为了评估神经损伤后观察到的快速基因诱导是否涉及损伤激活的MAP激酶级联反应，采用离体模型进行了实验。将坐骨神经节段在含氧的克雷布斯-林格缓冲液中孵育。 MAP激酶在15分钟时被激活，并在6小时后保持活性。还观察到了神经生长因子（NGF），白介素6（IL-6），白血病抑制因子（LIF）和2型（D2）和3型（D3）脱碘酶的mRNA诱导。因此，离体模型模仿了神经切片后动物中发生的事件。最后，在存在Erk1 / 2活化（U0126）和p38MAP激酶活性（SB203580）的特异性抑制剂的情况下孵育神经节段。 U0126抑制D3，LIF并在较小程度上抑制NGF mRNA的诱导，但不显着影响D2和IL-6 mRNA的诱导。 SB203580抑制D3和LIF基因的表达。我们得出的结论是，由神经横断激活的MAP激酶级联反应与神经中的快速基因诱导有关。

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