Peripheral HMGB1-induced hyperalgesia in mice: Redox state-dependent distinct roles of RAGE and TLR4

Daichi Yamasoba, Maho Tsubota, Risa Domoto, Fumiko Sekiguchi, Hiroyuki Nishikawa, Keyue Liu, Masahiro Nishibori, Hiroyasu Ishikura, Tetsushi Yamamoto, Atsushi Taga, Atsufumi Kawabata

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Nuclear HMGB1 that contains 3 cysteine residues is acetylated and secreted to the extracellular space, promoting inflammation via multiple molecules such as RAGE and TLR4. We thus evaluated and characterized the redox state-dependent effects of peripheral HMGB1 on nociception. Intraplantar (i.pl.) administration of bovine thymus-derived HMGB1 (bt-HMGB1), all-thiol HMGB1 (at-HMGB1) or disulfide HMGB1 (ds-HMGB1) caused long-lasting mechanical hyperalgesia in mice. The hyperalgesia following i.pl. bt-HMGB1 or at-HMGB1 was attenuated by RAGE inhibitors, while the ds-HMGB1-induced hyperalgesia was abolished by a TLR4 antagonist. Thus, nociceptive processing by peripheral HMGB1 is considered dependent on its redox states.

Original languageEnglish
Pages (from-to)139-142
Number of pages4
JournalJournal of Pharmacological Sciences
Volume130
Issue number2
DOIs
Publication statusPublished - Feb 1 2016

Keywords

  • High mobility group box 1
  • Pain
  • Redox state

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology

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    Yamasoba, D., Tsubota, M., Domoto, R., Sekiguchi, F., Nishikawa, H., Liu, K., Nishibori, M., Ishikura, H., Yamamoto, T., Taga, A., & Kawabata, A. (2016). Peripheral HMGB1-induced hyperalgesia in mice: Redox state-dependent distinct roles of RAGE and TLR4. Journal of Pharmacological Sciences, 130(2), 139-142. https://doi.org/10.1016/j.jphs.2016.01.005