Show simple item record Botz, Bálint Kemény, Ágnes Brunner SM Locker F Csepregi, Janka Zsófia Mócsai, Attila Pintér, Erika McDougall JJ Kofler B Helyes, Zsuzsanna 2018-09-19T09:14:41Z 2018-09-19T09:14:41Z 2016
dc.identifier 84960153108
dc.identifier.citation pagination=260-269; journalVolume=59; journalIssueNumber=2; journalTitle=JOURNAL OF MOLECULAR NEUROSCIENCE;
dc.identifier.uri doi:10.1007/s12031-016-0732-9
dc.description.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 (GAL1-3), GAL3 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 GAL3 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, GAL3 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 GAL3 receptor. Our findings suggest that GAL3 has anti-inflammatory properties in joints by inhibiting vascular hyperpermeability and consequent edema formation.
dc.relation.ispartof urn:issn:0895-8696
dc.title Lack of Galanin 3 Receptor Aggravates Murine Autoimmune Arthritis
dc.type Journal Article 2018-02-16T12:58:44Z
dc.language.rfc3066 en
dc.identifier.mtmt 3041989
dc.identifier.wos 000380720600010
dc.identifier.pubmed 26941032
dc.contributor.department PTE/SZKK/Molekuláris farmakológia kutatócsoport
dc.contributor.department SE/AOK/I/ÉI/MTA-SE Lendület Gyulladásélettani Kutatócsoport
dc.contributor.department SE/AOK/I/Élettani Intézet
dc.contributor.institution Pécsi Tudományegyetem
dc.contributor.institution Semmelweis Egyetem

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