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http://purl.uniprot.org/citations/16154213http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16154213http://www.w3.org/2000/01/rdf-schema#comment"

Background

CD26 is a multifunctional cell surface glycoprotein expressed by T and B cells. It exhibits a dipeptidyl-peptidase activity (DPP-IV) that cleaves the penultimate proline from the N-terminus of polypeptides, thereby regulating their activity and concentration.

Methods

Using CD26-/-mice resulting from targeted inactivation of the gene, we examined the consequences of a DPP-IV defect on behavioural response to nociceptive stimuli and concentration of the pain modulator peptides substance P (SP) and endomorphin 2, two DPP-IV substrates.

Results

CD26 inactivation induced a three-fold decrease in circulating endopeptidase activity while that found in brain extracts was normal, albeit very weak. CD26-/-mice had high SP concentrations in plasma (3.4+/-1 pg/ml versus 1.5+/-0.3 pg/ml, P<10(-3)) but not in brain extracts (35+/-12 pg/ml versus 32+/-9 pg/ml, P>0.05). Endomorphin-2 levels in the two groups were in the same range for plasma and brain extracts. CD26-/-mice displayed short latencies to nociceptive stimuli (hot plate test: 6.6+/-1.2 s versus 8.6+/-1.5 s, P<10(-4); tail pinch test: 3.1+/-0.6 s versus 4.2+/-0.8 s, P<10(-3)). Administration of an SP (NK1) receptor antagonist or DPP-IV to CD26-/-mice normalised latencies. DPP-IV inhibitors decreased latencies only in CD26+/+ mice.

Conclusions

Our observations represent the first fundamental evidence showing that DPP-IV influences pain perception via modulation of the peripheral SP concentration. Our work also highlights the role of peripheral NK1 receptors in nociception."xsd:string
http://purl.uniprot.org/citations/16154213http://purl.org/dc/terms/identifier"doi:10.1016/j.bbr.2005.08.003"xsd:string
http://purl.uniprot.org/citations/16154213http://purl.uniprot.org/core/author"Marguet D."xsd:string
http://purl.uniprot.org/citations/16154213http://purl.uniprot.org/core/author"Fenouillet E."xsd:string
http://purl.uniprot.org/citations/16154213http://purl.uniprot.org/core/author"Devaux C."xsd:string
http://purl.uniprot.org/citations/16154213http://purl.uniprot.org/core/author"Sauze N."xsd:string
http://purl.uniprot.org/citations/16154213http://purl.uniprot.org/core/author"Fajloun Z."xsd:string
http://purl.uniprot.org/citations/16154213http://purl.uniprot.org/core/author"Sabatier J.M."xsd:string
http://purl.uniprot.org/citations/16154213http://purl.uniprot.org/core/author"Carrega L."xsd:string
http://purl.uniprot.org/citations/16154213http://purl.uniprot.org/core/author"Guieu R."xsd:string
http://purl.uniprot.org/citations/16154213http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/16154213http://purl.uniprot.org/core/name"Behav Brain Res"xsd:string
http://purl.uniprot.org/citations/16154213http://purl.uniprot.org/core/pages"230-235"xsd:string
http://purl.uniprot.org/citations/16154213http://purl.uniprot.org/core/title"CD26 modulates nociception in mice via its dipeptidyl-peptidase IV activity."xsd:string
http://purl.uniprot.org/citations/16154213http://purl.uniprot.org/core/volume"166"xsd:string
http://purl.uniprot.org/citations/16154213http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/16154213
http://purl.uniprot.org/citations/16154213http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/16154213
http://purl.uniprot.org/uniprot/#_P28843-mappedCitation-16154213http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16154213
http://purl.uniprot.org/uniprot/#_Q3TR43-mappedCitation-16154213http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16154213
http://purl.uniprot.org/uniprot/Q3TR43http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/16154213
http://purl.uniprot.org/uniprot/P28843http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/16154213