| Literature DB >> 34924121 |
Risa Domoto1, Fumiko Sekiguchi1, Riki Kamaguchi1, Maiko Iemura1, Hiroki Yamanishi1, Maho Tsubota1, Dengli Wang2, Masahiro Nishibori2, Atsufumi Kawabata3.
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.Entities:
Keywords: ATP; Chemotherapy-induced peripheral neuropathy (CIPN); High mobility group box 1 (HMGB1); Neuroimmune crosstalk; Paclitaxel
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Year: 2021 PMID： 34924121 DOI： 10.1016/j.jphs.2021.11.003
Source DB: PubMed Journal: J Pharmacol Sci ISSN： 1347-8613 Impact factor: 3.337