Lack of Galanin 3 Receptor Aggravates Murine Autoimmune Arthritis
Neurogenic inflammation mediated by peptidergic sensory nerves has a crucial impact on the pathogenesis of various joint diseases. Galanin is a regulatory sensory neuropeptide, which has been shown to attenuate neurogenic inflammation, modulate neutrophil activation, and be involved in the developme...
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| Veröffentlicht in: | Journal of molecular neuroscience 2016-06, Vol.59 (2), p.260-269 |
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| creator | Botz, Bálint Kemény, Ágnes Brunner, Susanne M. Sternberg, Felix Csepregi, Janka Mócsai, Attila Pintér, Erika McDougall, Jason J. Kofler, Barbara Helyes, Zsuzsanna |
| description | Neurogenic inflammation mediated by peptidergic sensory nerves has a crucial impact on the pathogenesis of various joint diseases. Galanin is a regulatory sensory neuropeptide, which has been shown to attenuate neurogenic inflammation, modulate neutrophil activation, and be involved in the development of adjuvant arthritis, but our current understanding about its targets and physiological importance is incomplete. Among the receptors of galanin (GAL
1
–
3
), GAL
3
has been found to be the most abundantly expressed in the vasculature and on the surface of some immune cells. However, since there are minimal in vivo data on the role of GAL
3
in joint diseases, we analyzed its involvement in different inflammatory mechanisms of the K/BxN serum transfer-model of autoimmune arthritis employing
GAL
3
gene-deficient mice. After arthritis induction, GAL
3
knockouts demonstrated increased clinical disease severity and earlier hindlimb edema than wild types. Vascular hyperpermeability determined by in vivo fluorescence imaging was also elevated compared to the wild-type controls. However, neutrophil accumulation detected by in vivo luminescence imaging or arthritic mechanical hyperalgesia was not altered by the lack of the GAL
3
receptor. Our findings suggest that GAL
3
has anti-inflammatory properties in joints by inhibiting vascular hyperpermeability and consequent edema formation. |
| doi_str_mv | 10.1007/s12031-016-0732-9 |
| format | Article |
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1
–
3
), GAL
3
has been found to be the most abundantly expressed in the vasculature and on the surface of some immune cells. However, since there are minimal in vivo data on the role of GAL
3
in joint diseases, we analyzed its involvement in different inflammatory mechanisms of the K/BxN serum transfer-model of autoimmune arthritis employing
GAL
3
gene-deficient mice. After arthritis induction, GAL
3
knockouts demonstrated increased clinical disease severity and earlier hindlimb edema than wild types. Vascular hyperpermeability determined by in vivo fluorescence imaging was also elevated compared to the wild-type controls. However, neutrophil accumulation detected by in vivo luminescence imaging or arthritic mechanical hyperalgesia was not altered by the lack of the GAL
3
receptor. Our findings suggest that GAL
3
has anti-inflammatory properties in joints by inhibiting vascular hyperpermeability and consequent edema formation.</description><identifier>ISSN: 0895-8696</identifier><identifier>ISSN: 1559-1166</identifier><identifier>EISSN: 1559-1166</identifier><identifier>DOI: 10.1007/s12031-016-0732-9</identifier><identifier>PMID: 26941032</identifier><language>eng</language><publisher>New York: Springer New York</publisher><subject>Animals ; Anti-inflammatory agents ; Arthritis ; Arthritis - genetics ; Arthritis - metabolism ; Arthritis - pathology ; Autoimmune Diseases - genetics ; Autoimmune Diseases - metabolism ; Autoimmune Diseases - pathology ; Biomedicine ; Capillary Permeability ; Cell activation ; Cell Biology ; Cell surface ; Edema ; Edema - metabolism ; Endothelium, Vascular - metabolism ; Fluorescence ; Galanin ; Hindlimb - pathology ; Hyperalgesia ; Immune system ; In vivo methods and tests ; Inflammation ; Joint diseases ; Joints (anatomy) ; Leukocytes (neutrophilic) ; Male ; Medical imaging ; Mice ; Neurochemistry ; Neurology ; Neurosciences ; Neutrophils ; Neutrophils - metabolism ; Pain perception ; Pathogenesis ; Proteomics ; Receptor, Galanin, Type 3 - deficiency ; Receptor, Galanin, Type 3 - genetics ; Receptors ; Sensory neurons</subject><ispartof>Journal of molecular neuroscience, 2016-06, Vol.59 (2), p.260-269</ispartof><rights>The Author(s) 2016</rights><rights>The Author(s) 2016. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c531t-da1b626f1d6ff8936b55d5aea5a2a4921022942e1e9b6e7cf6b84b192d3ee2083</citedby><cites>FETCH-LOGICAL-c531t-da1b626f1d6ff8936b55d5aea5a2a4921022942e1e9b6e7cf6b84b192d3ee2083</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12031-016-0732-9$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12031-016-0732-9$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26941032$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Botz, Bálint</creatorcontrib><creatorcontrib>Kemény, Ágnes</creatorcontrib><creatorcontrib>Brunner, Susanne M.</creatorcontrib><creatorcontrib>Sternberg, Felix</creatorcontrib><creatorcontrib>Csepregi, Janka</creatorcontrib><creatorcontrib>Mócsai, Attila</creatorcontrib><creatorcontrib>Pintér, Erika</creatorcontrib><creatorcontrib>McDougall, Jason J.</creatorcontrib><creatorcontrib>Kofler, Barbara</creatorcontrib><creatorcontrib>Helyes, Zsuzsanna</creatorcontrib><title>Lack of Galanin 3 Receptor Aggravates Murine Autoimmune Arthritis</title><title>Journal of molecular neuroscience</title><addtitle>J Mol Neurosci</addtitle><addtitle>J Mol Neurosci</addtitle><description>Neurogenic inflammation mediated by peptidergic sensory nerves has a crucial impact on the pathogenesis of various joint diseases. Galanin is a regulatory sensory neuropeptide, which has been shown to attenuate neurogenic inflammation, modulate neutrophil activation, and be involved in the development of adjuvant arthritis, but our current understanding about its targets and physiological importance is incomplete. Among the receptors of galanin (GAL
1
–
3
), GAL
3
has been found to be the most abundantly expressed in the vasculature and on the surface of some immune cells. However, since there are minimal in vivo data on the role of GAL
3
in joint diseases, we analyzed its involvement in different inflammatory mechanisms of the K/BxN serum transfer-model of autoimmune arthritis employing
GAL
3
gene-deficient mice. After arthritis induction, GAL
3
knockouts demonstrated increased clinical disease severity and earlier hindlimb edema than wild types. Vascular hyperpermeability determined by in vivo fluorescence imaging was also elevated compared to the wild-type controls. However, neutrophil accumulation detected by in vivo luminescence imaging or arthritic mechanical hyperalgesia was not altered by the lack of the GAL
3
receptor. Our findings suggest that GAL
3
has anti-inflammatory properties in joints by inhibiting vascular hyperpermeability and consequent edema formation.</description><subject>Animals</subject><subject>Anti-inflammatory agents</subject><subject>Arthritis</subject><subject>Arthritis - genetics</subject><subject>Arthritis - metabolism</subject><subject>Arthritis - pathology</subject><subject>Autoimmune Diseases - genetics</subject><subject>Autoimmune Diseases - metabolism</subject><subject>Autoimmune Diseases - pathology</subject><subject>Biomedicine</subject><subject>Capillary Permeability</subject><subject>Cell activation</subject><subject>Cell Biology</subject><subject>Cell surface</subject><subject>Edema</subject><subject>Edema - metabolism</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Fluorescence</subject><subject>Galanin</subject><subject>Hindlimb - pathology</subject><subject>Hyperalgesia</subject><subject>Immune system</subject><subject>In vivo methods and tests</subject><subject>Inflammation</subject><subject>Joint diseases</subject><subject>Joints (anatomy)</subject><subject>Leukocytes (neutrophilic)</subject><subject>Male</subject><subject>Medical imaging</subject><subject>Mice</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Neutrophils</subject><subject>Neutrophils - metabolism</subject><subject>Pain perception</subject><subject>Pathogenesis</subject><subject>Proteomics</subject><subject>Receptor, Galanin, Type 3 - deficiency</subject><subject>Receptor, Galanin, Type 3 - genetics</subject><subject>Receptors</subject><subject>Sensory neurons</subject><issn>0895-8696</issn><issn>1559-1166</issn><issn>1559-1166</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkV1rFDEUhoNY7Fr9Ad7IgDfejOacfN8IS6mtsFIQvQ6Zmcw2dWeyJjOF_nszbC21YPEqgfOcNznnIeQN0A9AqfqYASmDmoKsqWJYm2dkBUKYGkDK52RFtRG1lkYek5c5X1OKwEG_IMcoDQfKcEXWG9f-rGJfnbudG8NYseqbb_1-iqlab7fJ3bjJ5-rrnMLoq_U8xTAM83JN01UKU8ivyFHvdtm_vjtPyI_PZ99PL-rN5fmX0_WmbgWDqe4cNBJlD53se22YbITohPNOOHTcIFBEw9GDN430qu1lo3kDBjvmPVLNTsinQ-5-bgbftX6cktvZfQqDS7c2umD_rozhym7jjeVacyFlCXh_F5Dir9nnyQ4ht35X5vZxzhY01Qq5ZP-BKoNKoTLLt949Qq_jnMayCVsQiVoZyZ-iliyUDAQWCg5Um2LOyff30wG1i3F7MG6LcbsYt6b0vH24lvuOP4oLgAcgl9K49enB0_9M_Q0MvbRa</recordid><startdate>20160601</startdate><enddate>20160601</enddate><creator>Botz, Bálint</creator><creator>Kemény, Ágnes</creator><creator>Brunner, Susanne M.</creator><creator>Sternberg, Felix</creator><creator>Csepregi, Janka</creator><creator>Mócsai, Attila</creator><creator>Pintér, Erika</creator><creator>McDougall, Jason J.</creator><creator>Kofler, Barbara</creator><creator>Helyes, Zsuzsanna</creator><general>Springer New York</general><general>Springer Nature B.V</general><general>Springer US</general><scope>C6C</scope><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>3V.</scope><scope>7QL</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>7T5</scope><scope>5PM</scope></search><sort><creationdate>20160601</creationdate><title>Lack of Galanin 3 Receptor Aggravates Murine Autoimmune Arthritis</title><author>Botz, Bálint ; Kemény, Ágnes ; Brunner, Susanne M. ; Sternberg, Felix ; Csepregi, Janka ; Mócsai, Attila ; Pintér, Erika ; McDougall, Jason J. ; Kofler, Barbara ; Helyes, Zsuzsanna</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c531t-da1b626f1d6ff8936b55d5aea5a2a4921022942e1e9b6e7cf6b84b192d3ee2083</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Anti-inflammatory agents</topic><topic>Arthritis</topic><topic>Arthritis - genetics</topic><topic>Arthritis - metabolism</topic><topic>Arthritis - pathology</topic><topic>Autoimmune Diseases - genetics</topic><topic>Autoimmune Diseases - metabolism</topic><topic>Autoimmune Diseases - pathology</topic><topic>Biomedicine</topic><topic>Capillary Permeability</topic><topic>Cell activation</topic><topic>Cell Biology</topic><topic>Cell surface</topic><topic>Edema</topic><topic>Edema - metabolism</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Fluorescence</topic><topic>Galanin</topic><topic>Hindlimb - pathology</topic><topic>Hyperalgesia</topic><topic>Immune system</topic><topic>In vivo methods and tests</topic><topic>Inflammation</topic><topic>Joint diseases</topic><topic>Joints (anatomy)</topic><topic>Leukocytes (neutrophilic)</topic><topic>Male</topic><topic>Medical imaging</topic><topic>Mice</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Neutrophils</topic><topic>Neutrophils - metabolism</topic><topic>Pain perception</topic><topic>Pathogenesis</topic><topic>Proteomics</topic><topic>Receptor, Galanin, Type 3 - 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Academic</collection><collection>Immunology Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of molecular neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Botz, Bálint</au><au>Kemény, Ágnes</au><au>Brunner, Susanne M.</au><au>Sternberg, Felix</au><au>Csepregi, Janka</au><au>Mócsai, Attila</au><au>Pintér, Erika</au><au>McDougall, Jason J.</au><au>Kofler, Barbara</au><au>Helyes, Zsuzsanna</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lack of Galanin 3 Receptor Aggravates Murine Autoimmune Arthritis</atitle><jtitle>Journal of molecular neuroscience</jtitle><stitle>J Mol Neurosci</stitle><addtitle>J Mol Neurosci</addtitle><date>2016-06-01</date><risdate>2016</risdate><volume>59</volume><issue>2</issue><spage>260</spage><epage>269</epage><pages>260-269</pages><issn>0895-8696</issn><issn>1559-1166</issn><eissn>1559-1166</eissn><abstract>Neurogenic inflammation mediated by peptidergic sensory nerves has a crucial impact on the pathogenesis of various joint diseases. Galanin is a regulatory sensory neuropeptide, which has been shown to attenuate neurogenic inflammation, modulate neutrophil activation, and be involved in the development of adjuvant arthritis, but our current understanding about its targets and physiological importance is incomplete. Among the receptors of galanin (GAL
1
–
3
), GAL
3
has been found to be the most abundantly expressed in the vasculature and on the surface of some immune cells. However, since there are minimal in vivo data on the role of GAL
3
in joint diseases, we analyzed its involvement in different inflammatory mechanisms of the K/BxN serum transfer-model of autoimmune arthritis employing
GAL
3
gene-deficient mice. After arthritis induction, GAL
3
knockouts demonstrated increased clinical disease severity and earlier hindlimb edema than wild types. Vascular hyperpermeability determined by in vivo fluorescence imaging was also elevated compared to the wild-type controls. However, neutrophil accumulation detected by in vivo luminescence imaging or arthritic mechanical hyperalgesia was not altered by the lack of the GAL
3
receptor. Our findings suggest that GAL
3
has anti-inflammatory properties in joints by inhibiting vascular hyperpermeability and consequent edema formation.</abstract><cop>New York</cop><pub>Springer New York</pub><pmid>26941032</pmid><doi>10.1007/s12031-016-0732-9</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of molecular neuroscience, 2016-06, Vol.59 (2), p.260-269 |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Animals Anti-inflammatory agents Arthritis Arthritis - genetics Arthritis - metabolism Arthritis - pathology Autoimmune Diseases - genetics Autoimmune Diseases - metabolism Autoimmune Diseases - pathology Biomedicine Capillary Permeability Cell activation Cell Biology Cell surface Edema Edema - metabolism Endothelium, Vascular - metabolism Fluorescence Galanin Hindlimb - pathology Hyperalgesia Immune system In vivo methods and tests Inflammation Joint diseases Joints (anatomy) Leukocytes (neutrophilic) Male Medical imaging Mice Neurochemistry Neurology Neurosciences Neutrophils Neutrophils - metabolism Pain perception Pathogenesis Proteomics Receptor, Galanin, Type 3 - deficiency Receptor, Galanin, Type 3 - genetics Receptors Sensory neurons |
| title | Lack of Galanin 3 Receptor Aggravates Murine Autoimmune Arthritis |
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