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. 2018 Mar 9;11:18–32. doi: 10.1016/j.molmet.2018.03.003

Figure 5.

Figure 5

Cyp2j4 deletion causes WAT dysfunction and a shunt in the AA pathway. (A) PPARγ and C/EBPα Western blot analyses in WT and Cyp2j4−/− WAT (STD vs. CAF) or aging (4-month vs.15-month old) conditions. (B) Schematic representation of AA and LA-derived eicosanoids. The Cyp450 pathway is shown in grey to illustrate the inhibition of Cyp2j4-derived EET production. All eicosanoids in green are up-regulated either in aging or CAF conditions in WAT from Cyp2j4−/− rats. For the quantitative data, see Supplementary Figure A.6A. (C) Schematic illustration of the quantitative lipidomics, proteomics, and RNA-seq datasets obtained from different tissues. The protein and mRNA levels of enzymes responsible for the generation of the eicosanoids detected in (B) were investigated in SVF LC-MS/MS, bone marrow-derived macrophage (BMDM) LC-MS/MS and RNA-seq. (D) Ptges3 and Cbr1 protein levels in WT and Cyp2j4−/− BMDMs by LC-MS/MS (n = 3 rats per group). (E) Ptgis protein levels in SVF by LC-MS/MS (n = 4 rats per group). (F) Schematic illustration of the AA COX pathway showing the enzymes that catalyze the synthesis of different prostaglandin species. (G) Graphical summary showing WAT homeostasis under aging and CAF in WT Cyp2j4−/− rats. Error bars are s.e.m.