Liver X Receptor [beta] Is Involved in Formalin-Induced Spontaneous Pain
Increasing evidence indicates that the liver X receptor(LXR) [beta] modulates inflammatory pain. However, the molecular mechanisms through which LXR[beta] modulates pain are unclear. Here, we found that LXR[beta]-null mice responded more strongly to acute noxious stimuli than wild-type (WT) litterma...
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| Veröffentlicht in: | Molecular neurobiology 2017-03, Vol.54 (2), p.1467 |
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| creator | Bao, Xiaohang Cai, Yulong Wang, Ying Zhao, Jinghui He, Xie Yu, Dan Huang, Jing Jing, Sheng Du, Zhiyong Yang, Tiande Warner, Margaret Gustafsson, Jan-ake Fan, Xiaotang |
| description | Increasing evidence indicates that the liver X receptor(LXR) [beta] modulates inflammatory pain. However, the molecular mechanisms through which LXR[beta] modulates pain are unclear. Here, we found that LXR[beta]-null mice responded more strongly to acute noxious stimuli than wild-type (WT) littermates (in the hot plate and Hargreaves tests) and had augmented tonic inflammatory pain (in the formalin test). This increased reactivity to inflammatory pain was accompanied by enhanced formalin-evoked Fos and pERK staining of second-order nociceptive neurons. Immunohistochemistry showed that the expression of CGRP, SP, and IB4 was increased in the lamina I-II of the lumbar dorsal horns in formalin-injected LXR[beta] knockout (KO) mice compared with the WT controls. In addition, LXR[beta] deletion in the mice enhanced the formalin-induced inflammation with more activated microglia and astrocytes in the spinal cord. Furthermore, the levels of pro-inflammatory cytokines (IL-1[beta] ,TNF-[alpha]) as well as NF[kappa]B in the formalin-injected paw were elevated by the loss of LXR[beta]. Taken together, these data indicate that LXR[beta] is involved in acute as well as inflammatory pain, and thus, it may be considered as a new target for the development of analgesics. |
| doi_str_mv | 10.1007/s12035-016-9737-1 |
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However, the molecular mechanisms through which LXR[beta] modulates pain are unclear. Here, we found that LXR[beta]-null mice responded more strongly to acute noxious stimuli than wild-type (WT) littermates (in the hot plate and Hargreaves tests) and had augmented tonic inflammatory pain (in the formalin test). This increased reactivity to inflammatory pain was accompanied by enhanced formalin-evoked Fos and pERK staining of second-order nociceptive neurons. Immunohistochemistry showed that the expression of CGRP, SP, and IB4 was increased in the lamina I-II of the lumbar dorsal horns in formalin-injected LXR[beta] knockout (KO) mice compared with the WT controls. In addition, LXR[beta] deletion in the mice enhanced the formalin-induced inflammation with more activated microglia and astrocytes in the spinal cord. Furthermore, the levels of pro-inflammatory cytokines (IL-1[beta] ,TNF-[alpha]) as well as NF[kappa]B in the formalin-injected paw were elevated by the loss of LXR[beta]. Taken together, these data indicate that LXR[beta] is involved in acute as well as inflammatory pain, and thus, it may be considered as a new target for the development of analgesics.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-016-9737-1</identifier><language>eng</language><publisher>Totowa: Springer Nature B.V</publisher><subject>Immunohistochemistry ; Ligands ; Neurobiology ; Neurons ; Pain ; Spinal cord ; Transcription factors</subject><ispartof>Molecular neurobiology, 2017-03, Vol.54 (2), p.1467</ispartof><rights>Molecular Neurobiology is a copyright of Springer, 2017.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Bao, Xiaohang</creatorcontrib><creatorcontrib>Cai, Yulong</creatorcontrib><creatorcontrib>Wang, Ying</creatorcontrib><creatorcontrib>Zhao, Jinghui</creatorcontrib><creatorcontrib>He, Xie</creatorcontrib><creatorcontrib>Yu, Dan</creatorcontrib><creatorcontrib>Huang, Jing</creatorcontrib><creatorcontrib>Jing, Sheng</creatorcontrib><creatorcontrib>Du, Zhiyong</creatorcontrib><creatorcontrib>Yang, Tiande</creatorcontrib><creatorcontrib>Warner, Margaret</creatorcontrib><creatorcontrib>Gustafsson, Jan-ake</creatorcontrib><creatorcontrib>Fan, Xiaotang</creatorcontrib><title>Liver X Receptor [beta] Is Involved in Formalin-Induced Spontaneous Pain</title><title>Molecular neurobiology</title><description>Increasing evidence indicates that the liver X receptor(LXR) [beta] modulates inflammatory pain. 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Taken together, these data indicate that LXR[beta] is involved in acute as well as inflammatory pain, and thus, it may be considered as a new target for the development of analgesics.</description><subject>Immunohistochemistry</subject><subject>Ligands</subject><subject>Neurobiology</subject><subject>Neurons</subject><subject>Pain</subject><subject>Spinal cord</subject><subject>Transcription factors</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNir0KwjAYAIMoWH8ewC3gHP2-Nm3SWRQLDqIOgohEG6GlJjVp-_w6-ABOB3dHyAxhgQBi6TGEKGaACUtFJBj2SIBxnDJEGfZJADKNmEi4HJKR9yVAGCKIgGx3RacdPdODfui6sY5e7rpRV5p5mpnOVp3OaWHoxrqXqgrDMpO3j6871tY0ymjberpXhZmQwVNVXk9_HJP5Zn1abVnt7LvVvrmVtnXmm24oExlzzpFH_10fSYRB2g</recordid><startdate>20170301</startdate><enddate>20170301</enddate><creator>Bao, Xiaohang</creator><creator>Cai, Yulong</creator><creator>Wang, Ying</creator><creator>Zhao, Jinghui</creator><creator>He, Xie</creator><creator>Yu, Dan</creator><creator>Huang, Jing</creator><creator>Jing, Sheng</creator><creator>Du, Zhiyong</creator><creator>Yang, Tiande</creator><creator>Warner, Margaret</creator><creator>Gustafsson, Jan-ake</creator><creator>Fan, Xiaotang</creator><general>Springer Nature B.V</general><scope>3V.</scope><scope>7QR</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope></search><sort><creationdate>20170301</creationdate><title>Liver X Receptor [beta] Is Involved in Formalin-Induced Spontaneous Pain</title><author>Bao, Xiaohang ; 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| subjects | Immunohistochemistry Ligands Neurobiology Neurons Pain Spinal cord Transcription factors |
| title | Liver X Receptor [beta] Is Involved in Formalin-Induced Spontaneous Pain |
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