IL-1β promotes neurite outgrowth by deactivating RhoA via p38 MAPK pathway
IL-1β promotes neurite outgrowth by deactivating RhoA via p38 MAPK pathway
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DOI：
10.1016/j.bbrc.2007.10.198
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发表时间：
2008-01-11
影响因子：
3.1
通讯作者：
Yoshikawa, Hideki
中科院分区：
文献类型：
--
作者：
Temporin, Ko;Tanaka, Hiroyuki;Yoshikawa, Hideki
神经系统损伤后，促炎细胞因子白细胞介素 1 β (IL-1 β) 的表达增加。一般来说，IL-1β 会诱发炎症，导致神经变性，同时也有报道称有几种神经刺激作用。尽管神经突生长是神经再生的重要一步，但 IL-1β 是否能利用它尚不清楚。现在我们研究它如何影响神经突的生长。坐骨神经损伤后，损伤部位周围雪旺细胞中 IL-1β 的表达增加，在损伤后 1 天达到峰值。在背根神经节 (DRG) 神经元和小脑颗粒神经元 (CGN) 中，通过添加髓磷脂相关糖蛋白 (MAG) 来抑制神经突生长，从而激活 RhoA。 IL-1 beta 通过使 RhoA 失活来克服 MAG 诱导的神经突生长抑制。细胞内信号传导实验表明，是 p38 MAPK 而不是核因子 kappa B (NF-kappa B) 介导了这种效应。这些发现表明，IL-1β 可能通过促进神经损伤后的神经突生长来促进神经再生。 (c) 2007 Elsevier Inc. 保留所有权利。
Expression of the pro-inflammatory cytokine interleukin-1 beta (IL-1 beta) is increased following the nervous system injury. Generally IL-1 beta induces inflammation, leading to neural degeneration, while several neuropoictic effects have also been reported. Although neurite outgrowth is an important step in nerve regeneration, whether IL-1 beta takes advantages on it is unclear. Now we examine how it affects neurite outgrowth. Following sciatic nerve injury, expression of IL-1 beta is increased in Schwann cells around the site of injury, peaking I day after injury. In dorsal root ganglion (DRG) neurons and cerebellar granule neurons (CGNs), neurite outgrowth is inhibited by the addition of myelin-associated glycoprotein (MAG), activating RhoA. IL-1 beta overcomes MAG-induced neurite outgrowth inhibition, by deactivating RhoA. Intracellular signaling experiments reveal that p38 MAPK, and not nuclear factor-kappa B (NF-kappa B), mediated this effect. These findings suggest that IL-1 beta may contribute to nerve regeneration by promoting neurite outgrowth following nerve injury. (c) 2007 Elsevier Inc. All rights reserved.