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Role of non-macrophage cell-derived HMGB1 in oxaliplatin-induced peripheral neuropathy and its prevention by the thrombin/thrombomodulin system in rodents: negative impact of anticoagulants

Tsubota, Maho; Fukuda, Ryotaro; Hayashi, Yusuke; Miyazaki, Takaya; Ueda, Shin; Yamashita, Rika; Koike, Nene; Sekiguchi, Fumiko; Wake, Hidenori; Wakatsuki, Shuji; Ujiie, Yuka; Araki, Toshiyuki; Nishibori, Masahiro; Kawabata, Atsufumi

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October 30, 2019

10.1186/s12974-019-1581-6

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Abstract:

Macrophage-derived high mobility group box 1 (HMGB1), a damage-associated molecular pattern (DAMP) protein, plays a key role in the development of chemotherapy-induced peripheral neuropathy (CIPN) caused by paclitaxel in rodents. Endothelial thrombomodulin (TM) promotes thrombin-induced degradation of HMGB1, and TMα, a recombinant human soluble TM, abolishes peripheral HMGB1-induced allodynia in mice. We thus examined whether HMGB1, particularly derived from macrophages, contributes to oxaliplatin-induced neuropathy in mice and analyzed the anti-neuropathic activity of the TM/thrombin system.