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Neuropeptide kyotorphin impacts on lipopolysaccharide-induced glucocorticoid-mediated inflammatory response : a molecular link to nociception, neuroprotection, and anti-inflammatory action

2017Journal article Restricted access
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dc.contributor.authorPerazzo, Juliana
dc.contributor.authorLima, Carla
dc.contributor.authorHeras, Montserrat
dc.contributor.authorBardají, Eduard
dc.contributor.authorFerreira, Mônica Lopes
dc.contributor.authorCastanho, Miguel A. R. B.
dc.date.accessioned2018-04-05T10:44:38Z
dc.date.available2018-04-05T10:44:38Z
dc.date.issued2017
dc.description© 2017 American Chemical Societypt_PT
dc.description.abstractNeuropeptide kyotorphin (KTP) is a potent analgesic if administered directly into the brain. In contrast, KTP-amide (KTP-NH2) is analgesic, neuroprotective, and anti-inflammatory following systemic administration, albeit its mechanism of action is unknown. The aim of this study was to shed light on the mechanism of action of KTP-NH2 at the molecular level. KTP-NH2 does not inhibit the enkephalinases angiotensin-converting-enzyme and dipeptidyl-peptidase 3. Intravital microscopy showed that KTP-NH2 decreased the number of rolling leukocytes in a mouse model of inflammation induced by lipopolysaccharide (LPS). Pretreatment with metyrapone abrogated the action of KTP-NH2. Interestingly, stimulating rolling leukocytes using CXCL-1 is also counteracted by the KTP-NH2, but this effect is not abrogated by metyrapone. We conclude that KTP-NH2 has dual action: a glucocorticoid-mediated action, which is dominant in the full-fledged LPS-induced inflammation model, and a glucocorticoid-independent mechanism, which is predominant in models in which leukocyte rolling is stimulated but inflammation is not totally developedpt_PT
dc.description.sponsorshipFCT-MCTES is acknowledged for Ph.D. fellowship SFRH/BD/52225/2013 to J.P. Marie Skłodowska-Curie Research and Innovation Staff Exchange (RISE) is acknowledged for funding: call H2020-MSCA-RISE-2014, Grant Agreement 644167, 2015-2019pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationACS Chem. Neurosci. 2017, 8, 1663−1667pt_PT
dc.identifier.doi10.1021/acschemneuro.7b00007pt_PT
dc.identifier.issn1948-7193
dc.identifier.urihttp://hdl.handle.net/10451/32603
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherAmerican Chemical Societypt_PT
dc.relationSFRH/BD/52225/2013pt_PT
dc.relation.publisherversionhttps://pubs.acs.org/journal/acncdmpt_PT
dc.subjectKyotorphinpt_PT
dc.subjectKyotorphin-amidept_PT
dc.subjectIntravital microscopypt_PT
dc.subjectGlucocorticoidspt_PT
dc.subjectMechanism of actionpt_PT
dc.subjectAnti-inflammatorypt_PT
dc.titleNeuropeptide kyotorphin impacts on lipopolysaccharide-induced glucocorticoid-mediated inflammatory response : a molecular link to nociception, neuroprotection, and anti-inflammatory actionpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage1667pt_PT
oaire.citation.issue8pt_PT
oaire.citation.startPage1663pt_PT
oaire.citation.titleACS Chemical Neurosciencept_PT
oaire.citation.volume8pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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