Neuropathic pain in rats with a partial sciatic nerve ligation is alleviated by intravenous injection of monoclonal antibody to high mobility group box-1
High mobility group box-1 (HMGB1) is associated with the pathogenesis of inflammatory diseases. A previous study reported that intravenous injection of anti-HMGB1 monoclonal antibody significantly attenuated brain edema in a rat model of stroke, possibly by attenuating glial activation. Peripheral n...
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| Veröffentlicht in: | PloS one 2013-08, Vol.8 (8), p.e73640-e73640 |
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| description | High mobility group box-1 (HMGB1) is associated with the pathogenesis of inflammatory diseases. A previous study reported that intravenous injection of anti-HMGB1 monoclonal antibody significantly attenuated brain edema in a rat model of stroke, possibly by attenuating glial activation. Peripheral nerve injury leads to increased activity of glia in the spinal cord dorsal horn. Thus, it is possible that the anti-HMGB1 antibody could also be efficacious in attenuating peripheral nerve injury-induced pain. Following partial sciatic nerve ligation (PSNL), rats were treated with either anti-HMGB1 or control IgG. Intravenous treatment with anti-HMGB1 monoclonal antibody (2 mg/kg) significantly ameliorated PSNL-induced hind paw tactile hypersensitivity at 7, 14 and 21 days, but not 3 days, after ligation, whereas control IgG had no effect on tactile hypersensitivity. The expression of HMGB1 protein in the spinal dorsal horn was significantly increased 7, 14 and 21 days after PSNL; the efficacy of the anti-HMGB1 antibody is likely related to the presence of HMGB1 protein. Also, the injury-induced translocation of HMGB1 from the nucleus to the cytosol occurred mainly in dorsal horn neurons and not in astrocytes and microglia, indicating a neuronal source of HMGB1. Markers of astrocyte (glial fibrillary acidic protein (GFAP)), microglia (ionized calcium binding adaptor molecule 1 (Iba1)) and spinal neuron (cFos) activity were greatly increased in the ipsilateral dorsal horn side compared to the sham-operated side 21 days after PSNL. Anti-HMGB1 monoclonal antibody treatment significantly decreased the injury-induced expression of cFos and Iba1, but not GFAP. The results demonstrate that nerve injury evokes the synthesis and release of HMGB1 from spinal neurons, facilitating the activity of both microglia and neurons, which in turn leads to symptoms of neuropathic pain. Thus, the targeting of HMGB1 could be a useful therapeutic strategy in the treatment of chronic pain. |
| doi_str_mv | 10.1371/journal.pone.0073640 |
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A previous study reported that intravenous injection of anti-HMGB1 monoclonal antibody significantly attenuated brain edema in a rat model of stroke, possibly by attenuating glial activation. Peripheral nerve injury leads to increased activity of glia in the spinal cord dorsal horn. Thus, it is possible that the anti-HMGB1 antibody could also be efficacious in attenuating peripheral nerve injury-induced pain. Following partial sciatic nerve ligation (PSNL), rats were treated with either anti-HMGB1 or control IgG. Intravenous treatment with anti-HMGB1 monoclonal antibody (2 mg/kg) significantly ameliorated PSNL-induced hind paw tactile hypersensitivity at 7, 14 and 21 days, but not 3 days, after ligation, whereas control IgG had no effect on tactile hypersensitivity. The expression of HMGB1 protein in the spinal dorsal horn was significantly increased 7, 14 and 21 days after PSNL; the efficacy of the anti-HMGB1 antibody is likely related to the presence of HMGB1 protein. Also, the injury-induced translocation of HMGB1 from the nucleus to the cytosol occurred mainly in dorsal horn neurons and not in astrocytes and microglia, indicating a neuronal source of HMGB1. Markers of astrocyte (glial fibrillary acidic protein (GFAP)), microglia (ionized calcium binding adaptor molecule 1 (Iba1)) and spinal neuron (cFos) activity were greatly increased in the ipsilateral dorsal horn side compared to the sham-operated side 21 days after PSNL. Anti-HMGB1 monoclonal antibody treatment significantly decreased the injury-induced expression of cFos and Iba1, but not GFAP. The results demonstrate that nerve injury evokes the synthesis and release of HMGB1 from spinal neurons, facilitating the activity of both microglia and neurons, which in turn leads to symptoms of neuropathic pain. Thus, the targeting of HMGB1 could be a useful therapeutic strategy in the treatment of chronic pain.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0073640</identifier><identifier>PMID: 23991202</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Antibodies, Monoclonal - administration & dosage ; Antibodies, Monoclonal - immunology ; Antibodies, Monoclonal - therapeutic use ; Antigen-antibody reactions ; Astrocytes ; Attenuation ; Biology ; Blotting, Western ; Brain ; Calcium ; Chromosomal proteins ; Chronic pain ; Cytokines ; Cytosol ; Dentistry ; Dorsal horn ; Edema ; Glial fibrillary acidic protein ; Health aspects ; Health sciences ; HMGB1 protein ; HMGB1 Protein - immunology ; Hypersensitivity ; Immunoglobulin G ; Inflammatory diseases ; Injection ; Injections, Intravenous ; Injuries ; Intermediate filament proteins ; Intravenous administration ; Kinases ; Laboratory animals ; Medicine ; Microglia ; Mobility ; Monoclonal antibodies ; Neuralgia - therapy ; Neuronal-glial interactions ; Neurons ; Neuropathy ; Pain ; Pain management ; Pathogenesis ; Peripheral neuropathy ; Permeability ; Pharmacology ; Protein transport ; Proteins ; Rats ; Rodents ; Sciatic nerve ; Sciatic Nerve - injuries ; Spinal cord ; Spinal cord injuries ; Stroke ; Studies ; Tactile ; Translocation ; Tumor necrosis factor-TNF</subject><ispartof>PloS one, 2013-08, Vol.8 (8), p.e73640-e73640</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Nakamura et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Nakamura et al 2013 Nakamura et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c736t-80de1b4df5ce8fbed4636a9ef2b5e21e12f65b41689b5189828c170c39928d43</citedby><cites>FETCH-LOGICAL-c736t-80de1b4df5ce8fbed4636a9ef2b5e21e12f65b41689b5189828c170c39928d43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3749159/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3749159/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2929,23870,27928,27929,53795,53797</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23991202$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Minami, Masabumi</contributor><creatorcontrib>Nakamura, Yoki</creatorcontrib><creatorcontrib>Morioka, Norimitsu</creatorcontrib><creatorcontrib>Abe, Hiromi</creatorcontrib><creatorcontrib>Zhang, Fang Fang</creatorcontrib><creatorcontrib>Hisaoka-Nakashima, Kazue</creatorcontrib><creatorcontrib>Liu, Keyue</creatorcontrib><creatorcontrib>Nishibori, Masahiro</creatorcontrib><creatorcontrib>Nakata, Yoshihiro</creatorcontrib><title>Neuropathic pain in rats with a partial sciatic nerve ligation is alleviated by intravenous injection of monoclonal antibody to high mobility group box-1</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>High mobility group box-1 (HMGB1) is associated with the pathogenesis of inflammatory diseases. A previous study reported that intravenous injection of anti-HMGB1 monoclonal antibody significantly attenuated brain edema in a rat model of stroke, possibly by attenuating glial activation. Peripheral nerve injury leads to increased activity of glia in the spinal cord dorsal horn. Thus, it is possible that the anti-HMGB1 antibody could also be efficacious in attenuating peripheral nerve injury-induced pain. Following partial sciatic nerve ligation (PSNL), rats were treated with either anti-HMGB1 or control IgG. Intravenous treatment with anti-HMGB1 monoclonal antibody (2 mg/kg) significantly ameliorated PSNL-induced hind paw tactile hypersensitivity at 7, 14 and 21 days, but not 3 days, after ligation, whereas control IgG had no effect on tactile hypersensitivity. The expression of HMGB1 protein in the spinal dorsal horn was significantly increased 7, 14 and 21 days after PSNL; the efficacy of the anti-HMGB1 antibody is likely related to the presence of HMGB1 protein. Also, the injury-induced translocation of HMGB1 from the nucleus to the cytosol occurred mainly in dorsal horn neurons and not in astrocytes and microglia, indicating a neuronal source of HMGB1. Markers of astrocyte (glial fibrillary acidic protein (GFAP)), microglia (ionized calcium binding adaptor molecule 1 (Iba1)) and spinal neuron (cFos) activity were greatly increased in the ipsilateral dorsal horn side compared to the sham-operated side 21 days after PSNL. Anti-HMGB1 monoclonal antibody treatment significantly decreased the injury-induced expression of cFos and Iba1, but not GFAP. The results demonstrate that nerve injury evokes the synthesis and release of HMGB1 from spinal neurons, facilitating the activity of both microglia and neurons, which in turn leads to symptoms of neuropathic pain. Thus, the targeting of HMGB1 could be a useful therapeutic strategy in the treatment of chronic pain.</description><subject>Animals</subject><subject>Antibodies, Monoclonal - administration & dosage</subject><subject>Antibodies, Monoclonal - immunology</subject><subject>Antibodies, Monoclonal - therapeutic use</subject><subject>Antigen-antibody reactions</subject><subject>Astrocytes</subject><subject>Attenuation</subject><subject>Biology</subject><subject>Blotting, Western</subject><subject>Brain</subject><subject>Calcium</subject><subject>Chromosomal proteins</subject><subject>Chronic pain</subject><subject>Cytokines</subject><subject>Cytosol</subject><subject>Dentistry</subject><subject>Dorsal horn</subject><subject>Edema</subject><subject>Glial fibrillary acidic protein</subject><subject>Health aspects</subject><subject>Health sciences</subject><subject>HMGB1 protein</subject><subject>HMGB1 Protein - immunology</subject><subject>Hypersensitivity</subject><subject>Immunoglobulin G</subject><subject>Inflammatory diseases</subject><subject>Injection</subject><subject>Injections, Intravenous</subject><subject>Injuries</subject><subject>Intermediate filament proteins</subject><subject>Intravenous administration</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Medicine</subject><subject>Microglia</subject><subject>Mobility</subject><subject>Monoclonal antibodies</subject><subject>Neuralgia - therapy</subject><subject>Neuronal-glial interactions</subject><subject>Neurons</subject><subject>Neuropathy</subject><subject>Pain</subject><subject>Pain management</subject><subject>Pathogenesis</subject><subject>Peripheral neuropathy</subject><subject>Permeability</subject><subject>Pharmacology</subject><subject>Protein transport</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rodents</subject><subject>Sciatic nerve</subject><subject>Sciatic Nerve - injuries</subject><subject>Spinal cord</subject><subject>Spinal cord injuries</subject><subject>Stroke</subject><subject>Studies</subject><subject>Tactile</subject><subject>Translocation</subject><subject>Tumor necrosis factor-TNF</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk22L1DAQx4so3nn6DUQDguiLXZM0fcgb4Th8WDg80MO3IU2nbZZsszbpevtR_LZOb_eOXbkX0kKTmd_MZP7NJMlLRucsLdiHpR-HXrv52vcwp7RIc0EfJadMpnyWc5o-PlifJM9CWFKapWWeP01OeCol45SfJn--wTj4tY6dNWStbU_wHXQM5LeNHdFoG6LVjgRjdUSmh2EDxNkWdx7pQLRzsEEn1KTaYngc9AZ6PwZcL8HcYr4hK9974zwemeg-2srXWxI96Wzboa-yzsYtaQc_rknlb2bsefKk0S7Ai_33LLn-_On64uvs8urL4uL8cmaw5TgraQ2sEnWTGSibCmqRp7mW0PAqA86A8SbPKsHyUlYZK2XJS8MKalABXtYiPUte79KunQ9qL2pQTKS0KDOWUiQWO6L2eqnWg13pYau8turW4IdWTRoZB4rLHGtQUzVCCgONlLnghairRmZYeKr2cV9trFZQG5jUckdJjz297VTrNyothGSZxATv9gkG_2uEENXKBgPO6R5Qcjw3l5xltMwRffMP-nB3e6rV2IDtG491zZRUnYuiZGUmiynX_AEKnxpW1uANbCzajwLeHwUgE-EmtnoMQS1-fP9_9urnMfv2gO1Au9gF78bploVjUOxAM_gQBmjuRWZUTQN0p4aaBkjtBwjDXh3-oPugu4lJ_wKoXhgD</recordid><startdate>20130821</startdate><enddate>20130821</enddate><creator>Nakamura, Yoki</creator><creator>Morioka, Norimitsu</creator><creator>Abe, Hiromi</creator><creator>Zhang, Fang Fang</creator><creator>Hisaoka-Nakashima, Kazue</creator><creator>Liu, Keyue</creator><creator>Nishibori, Masahiro</creator><creator>Nakata, Yoshihiro</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20130821</creationdate><title>Neuropathic pain in rats with a partial sciatic nerve ligation is alleviated by intravenous injection of monoclonal antibody to high mobility group box-1</title><author>Nakamura, Yoki ; Morioka, Norimitsu ; Abe, Hiromi ; Zhang, Fang Fang ; Hisaoka-Nakashima, Kazue ; Liu, Keyue ; Nishibori, Masahiro ; Nakata, Yoshihiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c736t-80de1b4df5ce8fbed4636a9ef2b5e21e12f65b41689b5189828c170c39928d43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Antibodies, Monoclonal - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nakamura, Yoki</au><au>Morioka, Norimitsu</au><au>Abe, Hiromi</au><au>Zhang, Fang Fang</au><au>Hisaoka-Nakashima, Kazue</au><au>Liu, Keyue</au><au>Nishibori, Masahiro</au><au>Nakata, Yoshihiro</au><au>Minami, Masabumi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuropathic pain in rats with a partial sciatic nerve ligation is alleviated by intravenous injection of monoclonal antibody to high mobility group box-1</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-08-21</date><risdate>2013</risdate><volume>8</volume><issue>8</issue><spage>e73640</spage><epage>e73640</epage><pages>e73640-e73640</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>High mobility group box-1 (HMGB1) is associated with the pathogenesis of inflammatory diseases. A previous study reported that intravenous injection of anti-HMGB1 monoclonal antibody significantly attenuated brain edema in a rat model of stroke, possibly by attenuating glial activation. Peripheral nerve injury leads to increased activity of glia in the spinal cord dorsal horn. Thus, it is possible that the anti-HMGB1 antibody could also be efficacious in attenuating peripheral nerve injury-induced pain. Following partial sciatic nerve ligation (PSNL), rats were treated with either anti-HMGB1 or control IgG. Intravenous treatment with anti-HMGB1 monoclonal antibody (2 mg/kg) significantly ameliorated PSNL-induced hind paw tactile hypersensitivity at 7, 14 and 21 days, but not 3 days, after ligation, whereas control IgG had no effect on tactile hypersensitivity. The expression of HMGB1 protein in the spinal dorsal horn was significantly increased 7, 14 and 21 days after PSNL; the efficacy of the anti-HMGB1 antibody is likely related to the presence of HMGB1 protein. Also, the injury-induced translocation of HMGB1 from the nucleus to the cytosol occurred mainly in dorsal horn neurons and not in astrocytes and microglia, indicating a neuronal source of HMGB1. Markers of astrocyte (glial fibrillary acidic protein (GFAP)), microglia (ionized calcium binding adaptor molecule 1 (Iba1)) and spinal neuron (cFos) activity were greatly increased in the ipsilateral dorsal horn side compared to the sham-operated side 21 days after PSNL. Anti-HMGB1 monoclonal antibody treatment significantly decreased the injury-induced expression of cFos and Iba1, but not GFAP. The results demonstrate that nerve injury evokes the synthesis and release of HMGB1 from spinal neurons, facilitating the activity of both microglia and neurons, which in turn leads to symptoms of neuropathic pain. Thus, the targeting of HMGB1 could be a useful therapeutic strategy in the treatment of chronic pain.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23991202</pmid><doi>10.1371/journal.pone.0073640</doi><tpages>e73640</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2013-08, Vol.8 (8), p.e73640-e73640 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1430785130 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Animals Antibodies, Monoclonal - administration & dosage Antibodies, Monoclonal - immunology Antibodies, Monoclonal - therapeutic use Antigen-antibody reactions Astrocytes Attenuation Biology Blotting, Western Brain Calcium Chromosomal proteins Chronic pain Cytokines Cytosol Dentistry Dorsal horn Edema Glial fibrillary acidic protein Health aspects Health sciences HMGB1 protein HMGB1 Protein - immunology Hypersensitivity Immunoglobulin G Inflammatory diseases Injection Injections, Intravenous Injuries Intermediate filament proteins Intravenous administration Kinases Laboratory animals Medicine Microglia Mobility Monoclonal antibodies Neuralgia - therapy Neuronal-glial interactions Neurons Neuropathy Pain Pain management Pathogenesis Peripheral neuropathy Permeability Pharmacology Protein transport Proteins Rats Rodents Sciatic nerve Sciatic Nerve - injuries Spinal cord Spinal cord injuries Stroke Studies Tactile Translocation Tumor necrosis factor-TNF |
| title | Neuropathic pain in rats with a partial sciatic nerve ligation is alleviated by intravenous injection of monoclonal antibody to high mobility group box-1 |
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