RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/27488890http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/27488890http://www.w3.org/2000/01/rdf-schema#comment"The relationship between soluble epoxide hydrolase (sEH) and coronary reactive hyperemia (CRH) response to a brief ischemic insult is not known. Epoxyeicosatrienoic acids (EETs) exert cardioprotective effects in ischemia/reperfusion injury. sEH converts EETs into dihydroxyeicosatrienoic-acids (DHETs). Therefore, we hypothesized that knocking out sEH enhances CRH through modulation of oxylipin profiles, including an increase in EET/DHET ratio. Compared with sEH+/+, sEH-/- mice showed enhanced CRH, including greater repayment volume (RV; 28% higher, P < 0.001) and repayment/debt ratio (32% higher, P < 0.001). Oxylipins from the heart perfusates were analyzed by LC-MS/MS. The 14,15-EET/14,15-DHET ratio was 3.7-fold higher at baseline (P < 0.001) and 5.6-fold higher post-ischemia (P < 0.001) in sEH-/- compared with sEH+/+ mice. Likewise, the baseline 9,10- and 12,13-EpOME/DiHOME ratios were 3.2-fold (P < 0.01) and 3.7-fold (P < 0.001) higher, respectively in sEH-/- compared with sEH+/+ mice. 13-HODE was also significantly increased at baseline by 71% (P < 0.01) in sEH-/- vs. sEH+/+ mice. Levels of 5-, 11-, 12-, and 15-hydroxyeicosatetraenoic acids were not significantly different between the two strains (P > 0.05), but were decreased postischemia in both groups (P = 0.02, P = 0.04, P = 0.05, P = 0.03, respectively). Modulation of CRH by peroxisome proliferator-activated receptor gamma (PPARγ) was demonstrated using a PPARγ-antagonist (T0070907), which reduced repayment volume by 25% in sEH+/+ (P < 0.001) and 33% in sEH-/- mice (P < 0.01), and a PPARγ-agonist (rosiglitazone), which increased repayment volume by 37% in both sEH+/+ (P = 0.04) and sEH-/- mice (P = 0.04). l-NAME attenuated CRH in both sEH-/- and sEH+/+ These data demonstrate that genetic deletion of sEH resulted in an altered oxylipin profile, which may have led to an enhanced CRH response."xsd:string
http://purl.uniprot.org/citations/27488890http://purl.org/dc/terms/identifier"doi:10.1152/ajpregu.00237.2016"xsd:string
http://purl.uniprot.org/citations/27488890http://purl.uniprot.org/core/author"Edin M.L."xsd:string
http://purl.uniprot.org/citations/27488890http://purl.uniprot.org/core/author"Zeldin D.C."xsd:string
http://purl.uniprot.org/citations/27488890http://purl.uniprot.org/core/author"Hanif A."xsd:string
http://purl.uniprot.org/citations/27488890http://purl.uniprot.org/core/author"Morisseau C."xsd:string
http://purl.uniprot.org/citations/27488890http://purl.uniprot.org/core/author"Nayeem M.A."xsd:string
http://purl.uniprot.org/citations/27488890http://purl.uniprot.org/core/date"2016"xsd:gYear
http://purl.uniprot.org/citations/27488890http://purl.uniprot.org/core/name"Am J Physiol Regul Integr Comp Physiol"xsd:string
http://purl.uniprot.org/citations/27488890http://purl.uniprot.org/core/pages"R676-R688"xsd:string
http://purl.uniprot.org/citations/27488890http://purl.uniprot.org/core/title"Deletion of soluble epoxide hydrolase enhances coronary reactive hyperemia in isolated mouse heart: role of oxylipins and PPARgamma."xsd:string
http://purl.uniprot.org/citations/27488890http://purl.uniprot.org/core/volume"311"xsd:string
http://purl.uniprot.org/citations/27488890http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/27488890
http://purl.uniprot.org/citations/27488890http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/27488890
http://purl.uniprot.org/uniprot/#_A0A0N4SV67-mappedCitation-27488890http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27488890
http://purl.uniprot.org/uniprot/#_A0A0N4SVF8-mappedCitation-27488890http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27488890
http://purl.uniprot.org/uniprot/#_A0N0C8-mappedCitation-27488890http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27488890
http://purl.uniprot.org/uniprot/#_A0N0D0-mappedCitation-27488890http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27488890
http://purl.uniprot.org/uniprot/#_A8JYK8-mappedCitation-27488890http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27488890
http://purl.uniprot.org/uniprot/#_D0EPX6-mappedCitation-27488890http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27488890
http://purl.uniprot.org/uniprot/#_D0EPX7-mappedCitation-27488890http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27488890
http://purl.uniprot.org/uniprot/#_D0EPX9-mappedCitation-27488890http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27488890
http://purl.uniprot.org/uniprot/#_P37238-mappedCitation-27488890http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27488890
http://purl.uniprot.org/uniprot/#_M1VPI1-mappedCitation-27488890http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27488890