Artemin–GFRα3 interactions partially contribute to acute inflammatory hypersensitivity
•Artemin antibodies block its binding to GFRα3 and inhibit pRet signalling.•Artemin-induced CGRP secretion from rat DRG cultures is reduced by monoclonal antibodies.•Delayed administration of anti-artemin antibodies partially reverse inflammatory hypersensitivity in mice. The expression of artemin (...
Gespeichert in:
| Veröffentlicht in: | NEUROSCIENCE LETTERS 2013-06, Vol.545, p.23-28 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 28 |
|---|---|
| container_issue | |
| container_start_page | 23 |
| container_title | NEUROSCIENCE LETTERS |
| container_volume | 545 |
| creator | Thornton, Peter Hatcher, Jon P. Robinson, Ian Sargent, Becky Franzén, Bo Martino, Giovanni Kitching, Lisa Glover, Colin P. Anderson, Dina Forsmo-Bruce, Heidi Low, Choon Pei Cusdin, Fiona Dosanjh, Bhupinder Williams, Wendy Steffen, Ann-Charlott Thompson, Simon Eklund, Malin Lloyd, Chris Chessell, Iain Hughes, Jane |
| description | •Artemin antibodies block its binding to GFRα3 and inhibit pRet signalling.•Artemin-induced CGRP secretion from rat DRG cultures is reduced by monoclonal antibodies.•Delayed administration of anti-artemin antibodies partially reverse inflammatory hypersensitivity in mice.
The expression of artemin (ARTN), a glial cell line-derived neurotrophic factor (GDNF) family ligand, increases in pre-clinical models of nociception and recent evidence suggests this growth factor may play a causative role in inflammatory pain mechanisms. The aim of this study was to demonstrate functional inhibition of ARTN with monoclonal antibodies and to determine whether ARTN neutralisation could reverse inflammatory pain in mice. We show that monoclonal antibodies with high affinity to ARTN, completely inhibit ARTN-induced Ret and ERK activation in a human neuroblastoma cell line, and block capsaicin-induced CGRP secretion from primary rat DRG cultures. In addition, administration of anti-ARTN antibodies to mice provides a transient, partial reversal (41%) of FCA-induced mechanical hypersensitivity. Anti-ARTN antibodies had no effect on hypersensitivity in response to partial nerve ligation in mice. These data suggest that ARTN–GFRα3 interactions partially mediate early stage nociceptive signalling following an inflammatory insult. |
| doi_str_mv | 10.1016/j.neulet.2013.04.007 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_swepu</sourceid><recordid>TN_cdi_proquest_miscellaneous_1365055975</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S030439401300356X</els_id><sourcerecordid>1365055975</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4072-fb6f3e97f9197d5c2e377497736bdbffe2967d3f83d13b47cbb736a021985bcc3</originalsourceid><addsrcrecordid>eNp9kU2KFTEQx4MozpvRG4j00k23-ey8bIRhcMaBAUF04Sok6Qrm2V8m6ZHeeQdP4kU8hCcxj37O0lUVVb-qf1F_hF4Q3BBM2teHZoSlh9xQTFiDeYOxfIR2ZC9pLZWkj9EOM8xrpjg-Q-cpHTDGggj-FJ1R1mJGhdqhz5cxwxDGPz9-3lx_-P2LVWHMEI3LYRpTNZuYg-n7tXLTmGOwS4YqT5VxxySMvjfDYPIU1-rLOkNMMKaQw33I6zP0xJs-wfNTvECfrt9-vHpX372_ub26vKsdx-VUb1vPQEmviJKdcBSYlFxJyVrbWe-BqlZ2zO9ZR5jl0llbWgZTovbCOscuUL3tTd9hXqyeYxhMXPVkgj6VvpYMtKBK7WnhX238HKdvC6Ssh5Ac9L0ZYVqSJqwVWAglRUH5hro4pRTBPywnWB9N0Ae9maCPJmjMdTGhjL08KSx2gO5h6N_XC_BmA6D85T5A1MkFGB10IYLLupvC_xX-Ak1jnls</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1365055975</pqid></control><display><type>article</type><title>Artemin–GFRα3 interactions partially contribute to acute inflammatory hypersensitivity</title><source>Elsevier ScienceDirect Journals Complete - AutoHoldings</source><source>MEDLINE</source><creator>Thornton, Peter ; Hatcher, Jon P. ; Robinson, Ian ; Sargent, Becky ; Franzén, Bo ; Martino, Giovanni ; Kitching, Lisa ; Glover, Colin P. ; Anderson, Dina ; Forsmo-Bruce, Heidi ; Low, Choon Pei ; Cusdin, Fiona ; Dosanjh, Bhupinder ; Williams, Wendy ; Steffen, Ann-Charlott ; Thompson, Simon ; Eklund, Malin ; Lloyd, Chris ; Chessell, Iain ; Hughes, Jane</creator><creatorcontrib>Thornton, Peter ; Hatcher, Jon P. ; Robinson, Ian ; Sargent, Becky ; Franzén, Bo ; Martino, Giovanni ; Kitching, Lisa ; Glover, Colin P. ; Anderson, Dina ; Forsmo-Bruce, Heidi ; Low, Choon Pei ; Cusdin, Fiona ; Dosanjh, Bhupinder ; Williams, Wendy ; Steffen, Ann-Charlott ; Thompson, Simon ; Eklund, Malin ; Lloyd, Chris ; Chessell, Iain ; Hughes, Jane</creatorcontrib><description>•Artemin antibodies block its binding to GFRα3 and inhibit pRet signalling.•Artemin-induced CGRP secretion from rat DRG cultures is reduced by monoclonal antibodies.•Delayed administration of anti-artemin antibodies partially reverse inflammatory hypersensitivity in mice.
The expression of artemin (ARTN), a glial cell line-derived neurotrophic factor (GDNF) family ligand, increases in pre-clinical models of nociception and recent evidence suggests this growth factor may play a causative role in inflammatory pain mechanisms. The aim of this study was to demonstrate functional inhibition of ARTN with monoclonal antibodies and to determine whether ARTN neutralisation could reverse inflammatory pain in mice. We show that monoclonal antibodies with high affinity to ARTN, completely inhibit ARTN-induced Ret and ERK activation in a human neuroblastoma cell line, and block capsaicin-induced CGRP secretion from primary rat DRG cultures. In addition, administration of anti-ARTN antibodies to mice provides a transient, partial reversal (41%) of FCA-induced mechanical hypersensitivity. Anti-ARTN antibodies had no effect on hypersensitivity in response to partial nerve ligation in mice. These data suggest that ARTN–GFRα3 interactions partially mediate early stage nociceptive signalling following an inflammatory insult.</description><identifier>ISSN: 0304-3940</identifier><identifier>EISSN: 1872-7972</identifier><identifier>DOI: 10.1016/j.neulet.2013.04.007</identifier><identifier>PMID: 23603259</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>Animals ; Artemin ; DRG ; Ganglia, Spinal - metabolism ; Glial Cell Line-Derived Neurotrophic Factor Receptors - metabolism ; Growth factors ; Hot Temperature ; Hyperalgesia - physiopathology ; Male ; Nerve Tissue Proteins - metabolism ; Pain ; Protein Binding ; Rats ; Rats, Sprague-Dawley ; Signal Transduction</subject><ispartof>NEUROSCIENCE LETTERS, 2013-06, Vol.545, p.23-28</ispartof><rights>2013 Elsevier Ireland Ltd</rights><rights>Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4072-fb6f3e97f9197d5c2e377497736bdbffe2967d3f83d13b47cbb736a021985bcc3</citedby><cites>FETCH-LOGICAL-c4072-fb6f3e97f9197d5c2e377497736bdbffe2967d3f83d13b47cbb736a021985bcc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neulet.2013.04.007$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,778,782,883,3539,27913,27914,45984</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23603259$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:126898892$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Thornton, Peter</creatorcontrib><creatorcontrib>Hatcher, Jon P.</creatorcontrib><creatorcontrib>Robinson, Ian</creatorcontrib><creatorcontrib>Sargent, Becky</creatorcontrib><creatorcontrib>Franzén, Bo</creatorcontrib><creatorcontrib>Martino, Giovanni</creatorcontrib><creatorcontrib>Kitching, Lisa</creatorcontrib><creatorcontrib>Glover, Colin P.</creatorcontrib><creatorcontrib>Anderson, Dina</creatorcontrib><creatorcontrib>Forsmo-Bruce, Heidi</creatorcontrib><creatorcontrib>Low, Choon Pei</creatorcontrib><creatorcontrib>Cusdin, Fiona</creatorcontrib><creatorcontrib>Dosanjh, Bhupinder</creatorcontrib><creatorcontrib>Williams, Wendy</creatorcontrib><creatorcontrib>Steffen, Ann-Charlott</creatorcontrib><creatorcontrib>Thompson, Simon</creatorcontrib><creatorcontrib>Eklund, Malin</creatorcontrib><creatorcontrib>Lloyd, Chris</creatorcontrib><creatorcontrib>Chessell, Iain</creatorcontrib><creatorcontrib>Hughes, Jane</creatorcontrib><title>Artemin–GFRα3 interactions partially contribute to acute inflammatory hypersensitivity</title><title>NEUROSCIENCE LETTERS</title><addtitle>Neurosci Lett</addtitle><description>•Artemin antibodies block its binding to GFRα3 and inhibit pRet signalling.•Artemin-induced CGRP secretion from rat DRG cultures is reduced by monoclonal antibodies.•Delayed administration of anti-artemin antibodies partially reverse inflammatory hypersensitivity in mice.
The expression of artemin (ARTN), a glial cell line-derived neurotrophic factor (GDNF) family ligand, increases in pre-clinical models of nociception and recent evidence suggests this growth factor may play a causative role in inflammatory pain mechanisms. The aim of this study was to demonstrate functional inhibition of ARTN with monoclonal antibodies and to determine whether ARTN neutralisation could reverse inflammatory pain in mice. We show that monoclonal antibodies with high affinity to ARTN, completely inhibit ARTN-induced Ret and ERK activation in a human neuroblastoma cell line, and block capsaicin-induced CGRP secretion from primary rat DRG cultures. In addition, administration of anti-ARTN antibodies to mice provides a transient, partial reversal (41%) of FCA-induced mechanical hypersensitivity. Anti-ARTN antibodies had no effect on hypersensitivity in response to partial nerve ligation in mice. These data suggest that ARTN–GFRα3 interactions partially mediate early stage nociceptive signalling following an inflammatory insult.</description><subject>Animals</subject><subject>Artemin</subject><subject>DRG</subject><subject>Ganglia, Spinal - metabolism</subject><subject>Glial Cell Line-Derived Neurotrophic Factor Receptors - metabolism</subject><subject>Growth factors</subject><subject>Hot Temperature</subject><subject>Hyperalgesia - physiopathology</subject><subject>Male</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Pain</subject><subject>Protein Binding</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Signal Transduction</subject><issn>0304-3940</issn><issn>1872-7972</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU2KFTEQx4MozpvRG4j00k23-ey8bIRhcMaBAUF04Sok6Qrm2V8m6ZHeeQdP4kU8hCcxj37O0lUVVb-qf1F_hF4Q3BBM2teHZoSlh9xQTFiDeYOxfIR2ZC9pLZWkj9EOM8xrpjg-Q-cpHTDGggj-FJ1R1mJGhdqhz5cxwxDGPz9-3lx_-P2LVWHMEI3LYRpTNZuYg-n7tXLTmGOwS4YqT5VxxySMvjfDYPIU1-rLOkNMMKaQw33I6zP0xJs-wfNTvECfrt9-vHpX372_ub26vKsdx-VUb1vPQEmviJKdcBSYlFxJyVrbWe-BqlZ2zO9ZR5jl0llbWgZTovbCOscuUL3tTd9hXqyeYxhMXPVkgj6VvpYMtKBK7WnhX238HKdvC6Ssh5Ac9L0ZYVqSJqwVWAglRUH5hro4pRTBPywnWB9N0Ae9maCPJmjMdTGhjL08KSx2gO5h6N_XC_BmA6D85T5A1MkFGB10IYLLupvC_xX-Ak1jnls</recordid><startdate>20130617</startdate><enddate>20130617</enddate><creator>Thornton, Peter</creator><creator>Hatcher, Jon P.</creator><creator>Robinson, Ian</creator><creator>Sargent, Becky</creator><creator>Franzén, Bo</creator><creator>Martino, Giovanni</creator><creator>Kitching, Lisa</creator><creator>Glover, Colin P.</creator><creator>Anderson, Dina</creator><creator>Forsmo-Bruce, Heidi</creator><creator>Low, Choon Pei</creator><creator>Cusdin, Fiona</creator><creator>Dosanjh, Bhupinder</creator><creator>Williams, Wendy</creator><creator>Steffen, Ann-Charlott</creator><creator>Thompson, Simon</creator><creator>Eklund, Malin</creator><creator>Lloyd, Chris</creator><creator>Chessell, Iain</creator><creator>Hughes, Jane</creator><general>Elsevier Ireland Ltd</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>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope></search><sort><creationdate>20130617</creationdate><title>Artemin–GFRα3 interactions partially contribute to acute inflammatory hypersensitivity</title><author>Thornton, Peter ; Hatcher, Jon P. ; Robinson, Ian ; Sargent, Becky ; Franzén, Bo ; Martino, Giovanni ; Kitching, Lisa ; Glover, Colin P. ; Anderson, Dina ; Forsmo-Bruce, Heidi ; Low, Choon Pei ; Cusdin, Fiona ; Dosanjh, Bhupinder ; Williams, Wendy ; Steffen, Ann-Charlott ; Thompson, Simon ; Eklund, Malin ; Lloyd, Chris ; Chessell, Iain ; Hughes, Jane</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4072-fb6f3e97f9197d5c2e377497736bdbffe2967d3f83d13b47cbb736a021985bcc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Artemin</topic><topic>DRG</topic><topic>Ganglia, Spinal - metabolism</topic><topic>Glial Cell Line-Derived Neurotrophic Factor Receptors - metabolism</topic><topic>Growth factors</topic><topic>Hot Temperature</topic><topic>Hyperalgesia - physiopathology</topic><topic>Male</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Pain</topic><topic>Protein Binding</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Thornton, Peter</creatorcontrib><creatorcontrib>Hatcher, Jon P.</creatorcontrib><creatorcontrib>Robinson, Ian</creatorcontrib><creatorcontrib>Sargent, Becky</creatorcontrib><creatorcontrib>Franzén, Bo</creatorcontrib><creatorcontrib>Martino, Giovanni</creatorcontrib><creatorcontrib>Kitching, Lisa</creatorcontrib><creatorcontrib>Glover, Colin P.</creatorcontrib><creatorcontrib>Anderson, Dina</creatorcontrib><creatorcontrib>Forsmo-Bruce, Heidi</creatorcontrib><creatorcontrib>Low, Choon Pei</creatorcontrib><creatorcontrib>Cusdin, Fiona</creatorcontrib><creatorcontrib>Dosanjh, Bhupinder</creatorcontrib><creatorcontrib>Williams, Wendy</creatorcontrib><creatorcontrib>Steffen, Ann-Charlott</creatorcontrib><creatorcontrib>Thompson, Simon</creatorcontrib><creatorcontrib>Eklund, Malin</creatorcontrib><creatorcontrib>Lloyd, Chris</creatorcontrib><creatorcontrib>Chessell, Iain</creatorcontrib><creatorcontrib>Hughes, Jane</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>SwePub</collection><collection>SwePub Articles</collection><jtitle>NEUROSCIENCE LETTERS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Thornton, Peter</au><au>Hatcher, Jon P.</au><au>Robinson, Ian</au><au>Sargent, Becky</au><au>Franzén, Bo</au><au>Martino, Giovanni</au><au>Kitching, Lisa</au><au>Glover, Colin P.</au><au>Anderson, Dina</au><au>Forsmo-Bruce, Heidi</au><au>Low, Choon Pei</au><au>Cusdin, Fiona</au><au>Dosanjh, Bhupinder</au><au>Williams, Wendy</au><au>Steffen, Ann-Charlott</au><au>Thompson, Simon</au><au>Eklund, Malin</au><au>Lloyd, Chris</au><au>Chessell, Iain</au><au>Hughes, Jane</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Artemin–GFRα3 interactions partially contribute to acute inflammatory hypersensitivity</atitle><jtitle>NEUROSCIENCE LETTERS</jtitle><addtitle>Neurosci Lett</addtitle><date>2013-06-17</date><risdate>2013</risdate><volume>545</volume><spage>23</spage><epage>28</epage><pages>23-28</pages><issn>0304-3940</issn><eissn>1872-7972</eissn><abstract>•Artemin antibodies block its binding to GFRα3 and inhibit pRet signalling.•Artemin-induced CGRP secretion from rat DRG cultures is reduced by monoclonal antibodies.•Delayed administration of anti-artemin antibodies partially reverse inflammatory hypersensitivity in mice.
The expression of artemin (ARTN), a glial cell line-derived neurotrophic factor (GDNF) family ligand, increases in pre-clinical models of nociception and recent evidence suggests this growth factor may play a causative role in inflammatory pain mechanisms. The aim of this study was to demonstrate functional inhibition of ARTN with monoclonal antibodies and to determine whether ARTN neutralisation could reverse inflammatory pain in mice. We show that monoclonal antibodies with high affinity to ARTN, completely inhibit ARTN-induced Ret and ERK activation in a human neuroblastoma cell line, and block capsaicin-induced CGRP secretion from primary rat DRG cultures. In addition, administration of anti-ARTN antibodies to mice provides a transient, partial reversal (41%) of FCA-induced mechanical hypersensitivity. Anti-ARTN antibodies had no effect on hypersensitivity in response to partial nerve ligation in mice. These data suggest that ARTN–GFRα3 interactions partially mediate early stage nociceptive signalling following an inflammatory insult.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>23603259</pmid><doi>10.1016/j.neulet.2013.04.007</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0304-3940 |
| ispartof | NEUROSCIENCE LETTERS, 2013-06, Vol.545, p.23-28 |
| issn | 0304-3940 1872-7972 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1365055975 |
| source | Elsevier ScienceDirect Journals Complete - AutoHoldings; MEDLINE |
| subjects | Animals Artemin DRG Ganglia, Spinal - metabolism Glial Cell Line-Derived Neurotrophic Factor Receptors - metabolism Growth factors Hot Temperature Hyperalgesia - physiopathology Male Nerve Tissue Proteins - metabolism Pain Protein Binding Rats Rats, Sprague-Dawley Signal Transduction |
| title | Artemin–GFRα3 interactions partially contribute to acute inflammatory hypersensitivity |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-15T08%3A55%3A35IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_swepu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Artemin%E2%80%93GFR%CE%B13%20interactions%20partially%20contribute%20to%20acute%20inflammatory%20hypersensitivity&rft.jtitle=NEUROSCIENCE%20LETTERS&rft.au=Thornton,%20Peter&rft.date=2013-06-17&rft.volume=545&rft.spage=23&rft.epage=28&rft.pages=23-28&rft.issn=0304-3940&rft.eissn=1872-7972&rft_id=info:doi/10.1016/j.neulet.2013.04.007&rft_dat=%3Cproquest_swepu%3E1365055975%3C/proquest_swepu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1365055975&rft_id=info:pmid/23603259&rft_els_id=S030439401300356X&rfr_iscdi=true |