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. 2019 Nov 16;31:138–149. doi: 10.1016/j.molmet.2019.10.008

Figure 5.

Figure 5

Dysfunction of FPR2 impaired SPM biosynthesis with dysregulation of LOXs and overactivation of COXs in the infarcted LV post-MI. (A) Pie chart representing the distribution of SPMs in WT and FPR2−/− mice at post-MI d1 in the infarcted LV. Percentage of mean values for each SPM moiety identified is presented in the pie chart. (B) Arachidonic acid (AA)–derived metabolome in the infarcted LV of WT and FPR2−/− mice post-MI at d1. (C, D, E, F) Decreased levels of SPMs (RvD1, RvD4, MaR2, and LXA4) in the infarcted LV of FPR2−/− mice compared with WT at post-MI d1. (G, H, I) Representative multiple reaction monitoring chromatographs of DHA-derived resolvins, AA-derived prostaglandins, and leukotrienes and RvD4. Bar graphs representing LV mRNA expression of (J, K)LOXs and (L, M)COXs (COX-1 and COX-2) at d1 post-MI. Values are means ± SEM; n = 4 mice per group in MI and no-MI controls. Quantification and values are pg/50 mg of LV tissue from apex to base. The detection limit was ∼1 pg.