The HMGB1 signaling pathway activates the inflammatory response in Schwann cells.
The HMGB1 signaling pathway activates the inflammatory response in Schwann cells.
复制标题
HMGB 1信号通路激活雪旺细胞的炎症反应
DOI：
10.4103/1673-5374.167773
复制
发表时间：
2015-10
影响因子：
6.1
通讯作者：
Wang YJ
中科院分区：
文献类型：
--
作者：
Man LL;Liu F;Wang YJ;Song HH;Xu HB;Zhu ZW;Zhang Q;Wang YJ
雪旺细胞不仅是髓鞘细胞，而且还具有免疫细胞的功能，并表达许多先天模式识别受体，包括 Toll 样受体。周围神经损伤会激活施万细胞的炎症反应。然而，尚不清楚特定的内源性损伤相关分子模式分子是否参与神经损伤后的炎症反应。在本研究中，我们证明了一种关键的损伤相关分子模式分子，即高迁移率族蛋白 1 (HMGB1)，在大鼠坐骨神经轴突切除术后表达上调，并且我们显示了该蛋白与 Schw-ann 细胞的共定位。 HMGB1 单独不能增强 Toll 样受体或晚期糖基化终产物受体 (RAGE) 的表达，但能够促进雪旺细胞的迁移。当雪旺细胞用 HMGB1 与脂多糖一起处理时，Toll 样受体和 RAGE 以及炎症细胞因子的表达水平上调。我们的新发现表明，HMGB1 通路在周围神经损伤后激活雪旺细胞中的炎症反应。
Schwann cells are not only myelinating cells, but also function as immune cells and express numerous innate pattern recognition receptors, including the Toll-like receptors. Injury to peripheral nerves activates an inflammatory response in Schwann cells. However, it is unclear whether specific endogenous damage-associated molecular pattern molecules are involved in the inflammatory response following nerve injury. In the present study, we demonstrate that a key damage-associated molecular pattern molecule, high mobility group box 1 (HMGB1), is upregulated following rat sciatic nerve axotomy, and we show colocalization of the protein with Schw-ann cells. HMGB1 alone could not enhance expression of Toll-like receptors or the receptor for advanced glycation end products (RAGE), but was able to facilitate migration of Schwann cells. When Schwann cells were treated with HMGB1 together with lipopolysaccharide, the expression levels of Toll-like receptors and RAGE, as well as inflammatory cytokines were upregulated. Our novel findings demonstrate that the HMGB1 pathway activates the inflammatory response in Schwann cells following peripheral nerve injury.