| http://purl.uniprot.org/citations/29526491 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/29526491 | http://www.w3.org/2000/01/rdf-schema#comment | "12/15 lipoxygenase (LOX) directs inflammation and lipid remodeling. However, the role of 12/15LOX in post-myocardial infarction (MI) left ventricular remodeling is unclear. To determine the role of 12/15LOX, 8-12 week-old C57BL/6 J wild-type (WT; n = 93) and 12/15LOX-/- (n = 97) mice were subjected to permanent coronary artery ligation and monitored at day (d)1 and d5 post-operatively. Post-MI d28 survival was measured in male and female mice. No-MI surgery mice were maintained as d0 naïve controls. 12/15LOX-/- mice exhibited higher survival rates with lower cardiac rupture and improved LV function as compared with WT post-MI. Compared to WT, neutrophils and macrophages in 12/15LOX-/- mice were polarized towards N2 and M2 phenotypes, respectively, with increased of expression mrc-1, ym-1, and arg-1 post-MI. 12/15LOX-/- mice exhibited lower levels of pro-inflammatory 12-(S)-hydroperoxyeicosatetraenoic acid (12(S)-HETE) and higher CYP2J-derived epoxyeicosatrienoic acids (EETs) levels. CYP2J-derived 5,6-, 8,9-, 11,12-, and 14,15-EETs activated macrophage-specific hemeoxygenase (HO)-1 marked with increases in F4/80+/Ly6Clow and F4/80+/CD206high cells at d5 post-MI in 12/15LOX-/- mice. In contrast, inhibition of HO-1 led to total mortality in 12/15LOX-/- mice by post-MI d5. 12/15LOX-/- mice exhibited reduced collagen density and lower α-smooth muscle actin (SMA) expression at d5 post-MI, indicating delayed or limited fibroblast-to-myofibroblast differentiation. In conclusion, genetic deletion of 12/15LOX reduces 12(S)-HETE and activates CYP2J-derived EETs to promote effective resolution of inflammation post-MI leading to reduced cardiac rupture, improved LV function, and better survival."xsd:string |
| http://purl.uniprot.org/citations/29526491 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.yjmcc.2018.03.004"xsd:string |
| http://purl.uniprot.org/citations/29526491 | http://purl.uniprot.org/core/author | "Barnes S."xsd:string |
| http://purl.uniprot.org/citations/29526491 | http://purl.uniprot.org/core/author | "Kabarowski J."xsd:string |
| http://purl.uniprot.org/citations/29526491 | http://purl.uniprot.org/core/author | "Prabhu S.D."xsd:string |
| http://purl.uniprot.org/citations/29526491 | http://purl.uniprot.org/core/author | "Limdi N.A."xsd:string |
| http://purl.uniprot.org/citations/29526491 | http://purl.uniprot.org/core/author | "Kain V."xsd:string |
| http://purl.uniprot.org/citations/29526491 | http://purl.uniprot.org/core/author | "Halade G.V."xsd:string |
| http://purl.uniprot.org/citations/29526491 | http://purl.uniprot.org/core/author | "Ingle K.A."xsd:string |
| http://purl.uniprot.org/citations/29526491 | http://purl.uniprot.org/core/date | "2018"xsd:gYear |
| http://purl.uniprot.org/citations/29526491 | http://purl.uniprot.org/core/name | "J Mol Cell Cardiol"xsd:string |
| http://purl.uniprot.org/citations/29526491 | http://purl.uniprot.org/core/pages | "70-80"xsd:string |
| http://purl.uniprot.org/citations/29526491 | http://purl.uniprot.org/core/title | "Genetic deletion of 12/15 lipoxygenase promotes effective resolution of inflammation following myocardial infarction."xsd:string |
| http://purl.uniprot.org/citations/29526491 | http://purl.uniprot.org/core/volume | "118"xsd:string |
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| http://purl.uniprot.org/uniprot/#_P39654-mappedCitation-29526491 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29526491 |
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