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http://purl.uniprot.org/citations/27778057http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/27778057http://www.w3.org/2000/01/rdf-schema#comment"

Objective and design

This study attempted to clarify the roles of endothelins and mechanisms associated with ETA/ETB receptors in mouse models of colitis.

Materials and methods

Colitis was induced by intracolonic administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS, 1.5 mg/animal) or dextran sulfate sodium (DSS, 3%). After colitis establishment, mice received Atrasentan (ETA receptor antagonist, 10 mg/kg), A-192621 (ETB receptor antagonist, 20 mg/kg) or Dexamethasone (1 mg/kg) and several inflammatory parameters were assessed, as well as mRNA levels for ET-1, ET-2 and ET receptors.

Results

Atrasentan treatment ameliorates TNBS- and DSS-induced colitis. In the TNBS model was observed reduction in macroscopic and microscopic score, colon weight, neutrophil influx, IL-1β, MIP-2 and keratinocyte chemoattractant (KC) levels, inhibition of adhesion molecules expression and restoration of IL-10 levels. However, A192621 treatment did not modify any parameter. ET-1 and ET-2 mRNA was decreased 24 h, but ET-2 mRNA was markedly increased at 48 h after TNBS. ET-2 was able to potentiate LPS-induced KC production in vitro. ETA and ETB receptors mRNA were increased at 24, 48 and 72 h after colitis induction.

Conclusions

Atrasentan treatment was effective in reducing the severity of colitis in DSS- and TNBS-treated mice, suggesting that ETA receptors might be a potential target for inflammatory bowel diseases."xsd:string
http://purl.uniprot.org/citations/27778057http://purl.org/dc/terms/identifier"doi:10.1007/s00011-016-1001-7"xsd:string
http://purl.uniprot.org/citations/27778057http://purl.uniprot.org/core/author"Calixto J.B."xsd:string
http://purl.uniprot.org/citations/27778057http://purl.uniprot.org/core/author"Rae G.A."xsd:string
http://purl.uniprot.org/citations/27778057http://purl.uniprot.org/core/author"Leite D.F."xsd:string
http://purl.uniprot.org/citations/27778057http://purl.uniprot.org/core/author"Chichorro J.G."xsd:string
http://purl.uniprot.org/citations/27778057http://purl.uniprot.org/core/author"Claudino R.F."xsd:string
http://purl.uniprot.org/citations/27778057http://purl.uniprot.org/core/author"Bento A.F."xsd:string
http://purl.uniprot.org/citations/27778057http://purl.uniprot.org/core/date"2017"xsd:gYear
http://purl.uniprot.org/citations/27778057http://purl.uniprot.org/core/name"Inflamm Res"xsd:string
http://purl.uniprot.org/citations/27778057http://purl.uniprot.org/core/pages"141-155"xsd:string
http://purl.uniprot.org/citations/27778057http://purl.uniprot.org/core/title"Potential role for ET-2 acting through ETA receptors in experimental colitis in mice."xsd:string
http://purl.uniprot.org/citations/27778057http://purl.uniprot.org/core/volume"66"xsd:string
http://purl.uniprot.org/citations/27778057http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/27778057
http://purl.uniprot.org/citations/27778057http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/27778057
http://purl.uniprot.org/uniprot/#_Q61614-mappedCitation-27778057http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27778057
http://purl.uniprot.org/uniprot/#_Q8BMW4-mappedCitation-27778057http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27778057
http://purl.uniprot.org/uniprot/Q61614http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/27778057
http://purl.uniprot.org/uniprot/Q8BMW4http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/27778057