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Neurokinin-1 receptor, a new modulator of lymphangiogenesis in obese-asthma phenotype

2013Journal article Open access
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dc.contributor.authorRamalho, Renata
dc.contributor.authorAlmeida, Joana
dc.contributor.authorFernandes, Rúben
dc.contributor.authorCosta, Raquel
dc.contributor.authorPirraco, Ana
dc.contributor.authorGuardão, Luísa
dc.contributor.authorDelgado, Luís
dc.contributor.authorMoreira, André
dc.contributor.authorSoares, Raquel
dc.date.accessioned2015-12-01T15:16:40Z
dc.date.available2020-01-01T01:30:11Z
dc.date.issued2013
dc.date.updated2013-07-25T20:47:35Z
dc.description.abstractAims Obesity and asthma are widely prevalent and associated disorders. Recent studies of our group revealed that Substance P (SP) is involved in pathophysiology of obese-asthma phenotype in mice through its selective NK1 receptor (NK1-R). Lymphangiogenesis is impaired in asthma and obesity, and SP activates contractile and inflammatory pathways in lymphatics. Our aim was to study whether NK1-R expression was involved in lymphangiogenesis on visceral (VAT) and subcutaneous (SAT) adipose tissues and in the lungs, in obese-allergen sensitized mice. Main methods Diet-induced obese and ovalbumin (OVA)-sensitized Balb/c mice were treated with a selective NK1-R antagonist (CJ 12,255, Pfizer Inc., USA) or placebo. Lymphatic structures (LYVE-1 +) and NK1-R expression were analyzed by immunohistochemistry. A semi-quantitative score methodology was used for NK1-R expression. Key findings Obesity and allergen-sensitization together increased the number of LYVE-1 + lymphatics in VAT and decreased it in SAT and lungs. NK1-R was mainly expressed on adipocyte membranes of VAT, blood vessel areas of SAT, and in lung epithelium. Obesity and allergen-sensitization combined increased the expression of NK1-R in VAT, SAT and lungs. NK1-R antagonist treatment reversed the effects observed in lymphangiogenesis in those tissues. Significance The obese-asthma phenotype in mice is accompanied by increased expression of NK1-R on adipose tissues and lung epithelium, reflecting that SP released during inflammation may act directly on these tissues. Blocking NK1-R affects lymphangiogenesis, implying a role of SP, with opposite physiological consequences in VAT, and in SAT and lungs. Our results provide a clue for a novel SP role in the obese-asthma phenotype.pt_PT
dc.identifier.doi10.1016/j.lfs.2013.06.010pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.22/7039
dc.language.isoengpt_PT
dc.publisherElsevierpt_PT
dc.relation.publisherversionhttp://www.sciencedirect.com/science/article/pii/S0024320513003378pt_PT
dc.subjectObesitypt_PT
dc.subjectAsthmapt_PT
dc.subjectAllergen-challengept_PT
dc.subjectNK1-Rpt_PT
dc.subjectSubstance Ppt_PT
dc.subjectLYVE-1pt_PT
dc.subjectLymphangiogenesispt_PT
dc.titleNeurokinin-1 receptor, a new modulator of lymphangiogenesis in obese-asthma phenotypept_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage177pt_PT
oaire.citation.startPage169pt_PT
oaire.citation.titleLife Sciencespt_PT
oaire.citation.volume93pt_PT
person.familyNameFernandes
person.givenNameRúben
person.identifier635792
person.identifier.ciencia-id0D1F-4090-E82A
person.identifier.orcid0000-0001-8933-3984
person.identifier.scopus-author-id57640135700
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublication9e6c397c-62d8-4a40-8ec7-ad05ae0ebcc4
relation.isAuthorOfPublication.latestForDiscovery9e6c397c-62d8-4a40-8ec7-ad05ae0ebcc4

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