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Gewählte Publikation:

Publikationstyp: Zeitschriftenaufsatz
Dokumentart: Originalarbeit

Publikationsjahr: 2016

AutorInnen: Botz, B; Kemény, Á; Brunner, SM; Locker, F; Csepregi, J; Mócsai, A; Pintér, E; McDougall, JJ; Kofler, B; Helyes, Z

Titel: Lack of Galanin 3 Receptor Aggravates Murine Autoimmune Arthritis.

Quelle: J Mol Neurosci. 2016; 59(2):260-269



Autor/innen der Vetmeduni Vienna:

Locker Felix

Diese Publikation wurde nicht im Namen der Vetmeduni Vienna erstellt und ist deshalb ausschließlich der persönlichen Publikationsliste des/der Autors/Autorin zugeordnet!


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.

Keywords Pubmed: Animals
Arthritis/genetics
Arthritis/metabolism*
Arthritis/pathology
Autoimmune Diseases/genetics
Autoimmune Diseases/metabolism*
Autoimmune Diseases/pathology
Capillary Permeability
Edema/metabolism
Endothelium, Vascular/metabolism
Hindlimb/pathology
Male
Mice
Neutrophils/metabolism
Receptor, Galanin, Type 3/deficiency
Receptor, Galanin, Type 3/genetics*


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