Role of neuron-derived ATP in paclitaxel-induced HMGB1 release from macrophages and peripheral neuropathy
Role of neuron-derived ATP in paclitaxel-induced HMGB1 release from macrophages and peripheral neuropathy
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神经元源性 ATP 在紫杉醇诱导巨噬细胞释放 HMGB1 和周围神经病变中的作用
DOI：
10.1016/j.jphs.2021.11.003
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发表时间：
2022
影响因子：
3.5
通讯作者：
Kawabata Atsufumi
中科院分区：
文献类型：
--
作者：
Domoto Risa;Sekiguchi Fumiko;Kamaguchi Riki;Iemura Maiko;Yamanishi Hiroki;Tsubota Maho;Wang Dengli;Nishibori Masahiro;Kawabata Atsufumi
我们研究了 ATP 和高迁移率族蛋白 1 (HMGB1) 在紫杉醇诱导的周围神经病变 (PIPN) 中的作用。小鼠中的 PIPN 可通过中和 HMGB1、巨噬细胞耗竭和 P2X7 或 P2X4 阻断来预防。紫杉醇和 ATP 可以从巨噬细胞样 RAW264.7 细胞中协同释放 HMGB1，但不能从神经元样 NG108-15 细胞中释放。通过与 NG108-15 细胞共培养，以依赖于 P2X7 或 P2X4 的方式加速紫杉醇诱导的 RAW264.7 细胞释放 HMGB1。紫杉醇从 NG108-15 细胞中释放 ATP，但不从 RAW264.7 细胞中释放 ATP。因此，PIPN被认为涉及通过神经元源性ATP激活P2X7和P2X4来加速巨噬细胞释放HMGB1。
We examined the role of ATP and high mobility group box 1 (HMGB1) in paclitaxel-induced peripheral neuropathy (PIPN). PIPN in mice was prevented by HMGB1 neutralization, macrophage depletion, and P2X7or P2X4blockade. Paclitaxel and ATP synergistically released HMGB1 from macrophage-like RAW264.7 cells, but not neuron-like NG108-15 cells. The paclitaxel-induced HMGB1 release from RAW264.7 cells was accelerated by co-culture with NG108-15 cells in a manner dependent on P2X7or P2X4. Paclitaxel released ATP from NG108-15 cells, but not RAW264.7 cells. Thus, PIPN is considered to involve acceleration of HMGB1 release from macrophages through P2X7and P2X4activation by neuron-derived ATP.