Role of neuron-derived ATP in paclitaxel-induced HMGB1 release from macrophages and peripheral neuropathy

Risa Domoto, Fumiko Sekiguchi, Riki Kamaguchi, Maiko Iemura, Hiroki Yamanishi, Maho Tsubota, Dengli Wang, Masahiro Nishibori, Atsufumi Kawabata

Research output: Contribution to journalArticlepeer-review

1 Citation (Scopus)

Abstract

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 P2X7 or P2X4 blockade. 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 P2X7 or 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 P2X7 and P2X4 activation by neuron-derived ATP.

Original languageEnglish
Pages (from-to)156-161
Number of pages6
JournalJournal of Pharmacological Sciences
Volume148
Issue number1
DOIs
Publication statusPublished - Jan 2022
Externally publishedYes

Keywords

  • ATP
  • Chemotherapy-induced peripheral neuropathy (CIPN)
  • High mobility group box 1 (HMGB1)
  • Neuroimmune crosstalk
  • Paclitaxel

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology

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