Perineural expression of high-mobility group box-1 contributes to long-lasting mechanical hypersensitivity via matrix metalloprotease-9 up-regulation in mice with painful peripheral neuropathy
Fang Fang Zhang, Norimitsu Morioka, Sakura Harano, Yoki Nakamura, Keyue Liu, Masahiro Nishibori, Kazue Hisaoka-Nakashima, Yoshihiro Nakata
High-mobility group box-1 (HMGB1) has been shown to be critical in the modulation of nociceptive transduction following a peripheral neuropathy. However, the precise role of peripherally expressed HMGB1 in neuropathic pain has yet to be fully elaborated. Following a partial sciatic nerve ligation (PSNL) in mice, a persistent ipsilateral up-regulation of HMGB1 was observed from 3 to 21 days after PSNL, in paralleled with a robust ipsilateral hind paw mechanical hypersensitivity. Increased HMGB1 was detected in both infiltrating macrophages and proliferating Schwann cells in the ipsilateral nerve 14 days following PSNL. Repeated perineural treatment with anti-HMGB1 antibody significantly ameliorated PSNL-induced mechanical hypersensitivity. Several pronociceptive molecules, including matrix metalloprotease-9 (MMP-9), tumor necrosis factor-α, interleukin-1β (IL-1β), and cyclooxygenase-2, were up-regulated in injured sciatic nerve 14 days following PSNL. Repeated perineural treatment with an anti-HMGB1 antibody significantly suppressed expression of MMP-9, but not other pronociceptive molecules. Perineural treatment with a selective MMP-9 inhibitor ameliorated PSNL-induced mechanical hypersensitivity. The current findings demonstrate that the maintenance of the neuropathic state following an injured nerve is dependent on the up-regulation of HMGB1 and MMP-9. Thus, blocking HMGB1 function in sciatic nerve could be a potent therapeutic strategy for the treatment of neuropathic pain. Increased peripheral high-mobility group box-1 (HMGB1) is involved in the modulation of nociceptive transduction following a peripheral neuropathy. Following nerve injury in mice, increased HMGB1 is detected in both infiltrating macrophages and proliferating Schwann cells in the ipsilateral nerve. Repeated perineural treatment with anti-HMGB1 antibody significantly ameliorates nerve injury-induced mechanical hypersensitivity, and suppresses expression of matrix metalloprotease-9 (MMP-9). The findings demonstrate that the maintenance of the neuropathic state following an injury nerve is dependent on the up-regulation of HMGB1 and MMP-9. Increased peripheral high-mobility group box-1 (HMGB1) is involved in the modulation of nociceptive transduction following a peripheral neuropathy. Following nerve injury in mice, increased HMGB1 is detected in both infiltrating macrophages and proliferating Schwann cells in the ipsilateral nerve. Repeated perineural treatment with anti-HMGB1 antibody significantly ameliorates nerve injury-induced mechanical hypersensitivity, and suppresses expression of matrix metalloprotease-9 (MMP-9). The findings demonstrate that the maintenance of the neuropathic state following an injury nerve is dependent on the up-regulation of HMGB1 and MMP-9.
Journal of Neurochemistry
https://doi.org/10.1111/jnc.13434
Allodynia
HMGB1
anti-HMGB1 monoclonal antibody
sciatic nerve
10.1111/jnc.13434
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Nociceptive Chemical Compounds 100%
Painful Neuropathy Medicine & Life Sciences 90%
Metalloproteases Medicine & Life Sciences 64%
Sciatic Nerve Medicine & Life Sciences 63%
Up-Regulation Medicine & Life Sciences 43%
Zhang, F. F., Morioka, N., Harano, S., Nakamura, Y., Liu, K., Nishibori, M., Hisaoka-Nakashima, K., & Nakata, Y. (2016). Perineural expression of high-mobility group box-1 contributes to long-lasting mechanical hypersensitivity via matrix metalloprotease-9 up-regulation in mice with painful peripheral neuropathy. Journal of Neurochemistry, 136(4), 837-850. https://doi.org/10.1111/jnc.13434
Perineural expression of high-mobility group box-1 contributes to long-lasting mechanical hypersensitivity via matrix metalloprotease-9 up-regulation in mice with painful peripheral neuropathy. / Zhang, Fang Fang; Morioka, Norimitsu; Harano, Sakura et al.
In: Journal of Neurochemistry, Vol. 136, No. 4, 01.02.2016, p. 837-850.
Zhang, FF, Morioka, N, Harano, S, Nakamura, Y, Liu, K, Nishibori, M, Hisaoka-Nakashima, K & Nakata, Y 2016, 'Perineural expression of high-mobility group box-1 contributes to long-lasting mechanical hypersensitivity via matrix metalloprotease-9 up-regulation in mice with painful peripheral neuropathy', Journal of Neurochemistry, vol. 136, no. 4, pp. 837-850. https://doi.org/10.1111/jnc.13434
Zhang FF, Morioka N, Harano S, Nakamura Y, Liu K, Nishibori M et al. Perineural expression of high-mobility group box-1 contributes to long-lasting mechanical hypersensitivity via matrix metalloprotease-9 up-regulation in mice with painful peripheral neuropathy. Journal of Neurochemistry. 2016 Feb 1;136(4):837-850. doi: 10.1111/jnc.13434
Zhang, Fang Fang ; Morioka, Norimitsu ; Harano, Sakura et al. / Perineural expression of high-mobility group box-1 contributes to long-lasting mechanical hypersensitivity via matrix metalloprotease-9 up-regulation in mice with painful peripheral neuropathy. In: Journal of Neurochemistry. 2016 ; Vol. 136, No. 4. pp. 837-850.
@article{1e14586cbb8249b9a18e089860b6311d,
title = "Perineural expression of high-mobility group box-1 contributes to long-lasting mechanical hypersensitivity via matrix metalloprotease-9 up-regulation in mice with painful peripheral neuropathy",
abstract = "High-mobility group box-1 (HMGB1) has been shown to be critical in the modulation of nociceptive transduction following a peripheral neuropathy. However, the precise role of peripherally expressed HMGB1 in neuropathic pain has yet to be fully elaborated. Following a partial sciatic nerve ligation (PSNL) in mice, a persistent ipsilateral up-regulation of HMGB1 was observed from 3 to 21 days after PSNL, in paralleled with a robust ipsilateral hind paw mechanical hypersensitivity. Increased HMGB1 was detected in both infiltrating macrophages and proliferating Schwann cells in the ipsilateral nerve 14 days following PSNL. Repeated perineural treatment with anti-HMGB1 antibody significantly ameliorated PSNL-induced mechanical hypersensitivity. Several pronociceptive molecules, including matrix metalloprotease-9 (MMP-9), tumor necrosis factor-α, interleukin-1β (IL-1β), and cyclooxygenase-2, were up-regulated in injured sciatic nerve 14 days following PSNL. Repeated perineural treatment with an anti-HMGB1 antibody significantly suppressed expression of MMP-9, but not other pronociceptive molecules. Perineural treatment with a selective MMP-9 inhibitor ameliorated PSNL-induced mechanical hypersensitivity. The current findings demonstrate that the maintenance of the neuropathic state following an injured nerve is dependent on the up-regulation of HMGB1 and MMP-9. Thus, blocking HMGB1 function in sciatic nerve could be a potent therapeutic strategy for the treatment of neuropathic pain. Increased peripheral high-mobility group box-1 (HMGB1) is involved in the modulation of nociceptive transduction following a peripheral neuropathy. Following nerve injury in mice, increased HMGB1 is detected in both infiltrating macrophages and proliferating Schwann cells in the ipsilateral nerve. Repeated perineural treatment with anti-HMGB1 antibody significantly ameliorates nerve injury-induced mechanical hypersensitivity, and suppresses expression of matrix metalloprotease-9 (MMP-9). The findings demonstrate that the maintenance of the neuropathic state following an injury nerve is dependent on the up-regulation of HMGB1 and MMP-9. Increased peripheral high-mobility group box-1 (HMGB1) is involved in the modulation of nociceptive transduction following a peripheral neuropathy. Following nerve injury in mice, increased HMGB1 is detected in both infiltrating macrophages and proliferating Schwann cells in the ipsilateral nerve. Repeated perineural treatment with anti-HMGB1 antibody significantly ameliorates nerve injury-induced mechanical hypersensitivity, and suppresses expression of matrix metalloprotease-9 (MMP-9). The findings demonstrate that the maintenance of the neuropathic state following an injury nerve is dependent on the up-regulation of HMGB1 and MMP-9.",
keywords = "Allodynia, HMGB1, MMP-9, anti-HMGB1 monoclonal antibody, sciatic nerve",
author = "Zhang, {Fang Fang} and Norimitsu Morioka and Sakura Harano and Yoki Nakamura and Keyue Liu and Masahiro Nishibori and Kazue Hisaoka-Nakashima and Yoshihiro Nakata",
note = "Publisher Copyright: {\textcopyright} 2015 International Society for Neurochemistry. Copyright: Copyright 2016 Elsevier B.V., All rights reserved.",
doi = "10.1111/jnc.13434",
journal = "Journal of Neurochemistry",
T1 - Perineural expression of high-mobility group box-1 contributes to long-lasting mechanical hypersensitivity via matrix metalloprotease-9 up-regulation in mice with painful peripheral neuropathy
AU - Zhang, Fang Fang
AU - Morioka, Norimitsu
AU - Harano, Sakura
AU - Nakamura, Yoki
AU - Liu, Keyue
AU - Nishibori, Masahiro
AU - Hisaoka-Nakashima, Kazue
AU - Nakata, Yoshihiro
N1 - Publisher Copyright: © 2015 International Society for Neurochemistry. Copyright: Copyright 2016 Elsevier B.V., All rights reserved.
N2 - High-mobility group box-1 (HMGB1) has been shown to be critical in the modulation of nociceptive transduction following a peripheral neuropathy. However, the precise role of peripherally expressed HMGB1 in neuropathic pain has yet to be fully elaborated. Following a partial sciatic nerve ligation (PSNL) in mice, a persistent ipsilateral up-regulation of HMGB1 was observed from 3 to 21 days after PSNL, in paralleled with a robust ipsilateral hind paw mechanical hypersensitivity. Increased HMGB1 was detected in both infiltrating macrophages and proliferating Schwann cells in the ipsilateral nerve 14 days following PSNL. Repeated perineural treatment with anti-HMGB1 antibody significantly ameliorated PSNL-induced mechanical hypersensitivity. Several pronociceptive molecules, including matrix metalloprotease-9 (MMP-9), tumor necrosis factor-α, interleukin-1β (IL-1β), and cyclooxygenase-2, were up-regulated in injured sciatic nerve 14 days following PSNL. Repeated perineural treatment with an anti-HMGB1 antibody significantly suppressed expression of MMP-9, but not other pronociceptive molecules. Perineural treatment with a selective MMP-9 inhibitor ameliorated PSNL-induced mechanical hypersensitivity. The current findings demonstrate that the maintenance of the neuropathic state following an injured nerve is dependent on the up-regulation of HMGB1 and MMP-9. Thus, blocking HMGB1 function in sciatic nerve could be a potent therapeutic strategy for the treatment of neuropathic pain. Increased peripheral high-mobility group box-1 (HMGB1) is involved in the modulation of nociceptive transduction following a peripheral neuropathy. Following nerve injury in mice, increased HMGB1 is detected in both infiltrating macrophages and proliferating Schwann cells in the ipsilateral nerve. Repeated perineural treatment with anti-HMGB1 antibody significantly ameliorates nerve injury-induced mechanical hypersensitivity, and suppresses expression of matrix metalloprotease-9 (MMP-9). The findings demonstrate that the maintenance of the neuropathic state following an injury nerve is dependent on the up-regulation of HMGB1 and MMP-9. Increased peripheral high-mobility group box-1 (HMGB1) is involved in the modulation of nociceptive transduction following a peripheral neuropathy. Following nerve injury in mice, increased HMGB1 is detected in both infiltrating macrophages and proliferating Schwann cells in the ipsilateral nerve. Repeated perineural treatment with anti-HMGB1 antibody significantly ameliorates nerve injury-induced mechanical hypersensitivity, and suppresses expression of matrix metalloprotease-9 (MMP-9). The findings demonstrate that the maintenance of the neuropathic state following an injury nerve is dependent on the up-regulation of HMGB1 and MMP-9.
AB - High-mobility group box-1 (HMGB1) has been shown to be critical in the modulation of nociceptive transduction following a peripheral neuropathy. However, the precise role of peripherally expressed HMGB1 in neuropathic pain has yet to be fully elaborated. Following a partial sciatic nerve ligation (PSNL) in mice, a persistent ipsilateral up-regulation of HMGB1 was observed from 3 to 21 days after PSNL, in paralleled with a robust ipsilateral hind paw mechanical hypersensitivity. Increased HMGB1 was detected in both infiltrating macrophages and proliferating Schwann cells in the ipsilateral nerve 14 days following PSNL. Repeated perineural treatment with anti-HMGB1 antibody significantly ameliorated PSNL-induced mechanical hypersensitivity. Several pronociceptive molecules, including matrix metalloprotease-9 (MMP-9), tumor necrosis factor-α, interleukin-1β (IL-1β), and cyclooxygenase-2, were up-regulated in injured sciatic nerve 14 days following PSNL. Repeated perineural treatment with an anti-HMGB1 antibody significantly suppressed expression of MMP-9, but not other pronociceptive molecules. Perineural treatment with a selective MMP-9 inhibitor ameliorated PSNL-induced mechanical hypersensitivity. The current findings demonstrate that the maintenance of the neuropathic state following an injured nerve is dependent on the up-regulation of HMGB1 and MMP-9. Thus, blocking HMGB1 function in sciatic nerve could be a potent therapeutic strategy for the treatment of neuropathic pain. Increased peripheral high-mobility group box-1 (HMGB1) is involved in the modulation of nociceptive transduction following a peripheral neuropathy. Following nerve injury in mice, increased HMGB1 is detected in both infiltrating macrophages and proliferating Schwann cells in the ipsilateral nerve. Repeated perineural treatment with anti-HMGB1 antibody significantly ameliorates nerve injury-induced mechanical hypersensitivity, and suppresses expression of matrix metalloprotease-9 (MMP-9). The findings demonstrate that the maintenance of the neuropathic state following an injury nerve is dependent on the up-regulation of HMGB1 and MMP-9. Increased peripheral high-mobility group box-1 (HMGB1) is involved in the modulation of nociceptive transduction following a peripheral neuropathy. Following nerve injury in mice, increased HMGB1 is detected in both infiltrating macrophages and proliferating Schwann cells in the ipsilateral nerve. Repeated perineural treatment with anti-HMGB1 antibody significantly ameliorates nerve injury-induced mechanical hypersensitivity, and suppresses expression of matrix metalloprotease-9 (MMP-9). The findings demonstrate that the maintenance of the neuropathic state following an injury nerve is dependent on the up-regulation of HMGB1 and MMP-9.
KW - Allodynia
KW - HMGB1
KW - MMP-9
KW - anti-HMGB1 monoclonal antibody
KW - sciatic nerve
U2 - 10.1111/jnc.13434
DO - 10.1111/jnc.13434
JO - Journal of Neurochemistry
JF - Journal of Neurochemistry