TY - JOUR
T1 - Peripheral HMGB1-induced hyperalgesia in mice
T2 - Redox state-dependent distinct roles of RAGE and TLR4
AU - Yamasoba, Daichi
AU - Tsubota, Maho
AU - Domoto, Risa
AU - Sekiguchi, Fumiko
AU - Nishikawa, Hiroyuki
AU - Liu, Keyue
AU - Nishibori, Masahiro
AU - Ishikura, Hiroyasu
AU - Yamamoto, Tetsushi
AU - Taga, Atsushi
AU - Kawabata, Atsufumi
N1 - Funding Information:
This work was supported by Japan Society for the Promotion of Science KAKENHI Grant Number 26460710 , and also in part by the Ministry of Education, Culture, Sports, Science, and Technology -Supported Program for the Strategic Research Foundation at Private Universities (2014-2018) ( S1411037 ).
Publisher Copyright:
© 2016 Japanese Pharmacological Society. Production and hosting by Elsevier B.V.
PY - 2016/2/1
Y1 - 2016/2/1
N2 - 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.
AB - 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.
KW - High mobility group box 1
KW - Pain
KW - Redox state
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U2 - 10.1016/j.jphs.2016.01.005
DO - 10.1016/j.jphs.2016.01.005
M3 - Article
C2 - 26883456
AN - SCOPUS:84957646711
VL - 130
SP - 139
EP - 142
JO - Journal of Pharmacological Sciences
JF - Journal of Pharmacological Sciences
SN - 1347-8648
IS - 2
ER -