Skip to main content
. Author manuscript; available in PMC: 2023 Oct 11.
Published in final edited form as: Sci Signal. 2023 Jul 11;16(793):eadd6527. doi: 10.1126/scisignal.add6527

Fig. 3. Loss of the C1P-cPLA2α interaction enhance trans-endothelial migration of primary neutrophils through the induction of 5-HETE and 5-oxo-ETE biosynthesis and OXER1 activation.

Fig. 3.

(A) Quantification of neutrophil trans-endothelial migration (NTEM) of primary neutrophils (PNs) from cPLA2α+/+, cPLA2αKI/KI, and cPLA2α−/− mice. (B) Eicosanoid profile of cytokine- and chemoattractant-activated neutrophils after 4 hours of NTEM. (C) Quantification of the eicosanoid, PGD2, PGE2, 5-HETE, and 5-oxo-ETE after 4 hours NTEM. (D) NTEM after 4 hours in the presence of vehicle (DMSO), the FLAP inhibitor MK886, the OXER1 antagonist Gue1654, and 5-HETE as indicated. (E) Quantification of eicosanoids in cPLA2α+/+ and cPLA2αKI/KI PNs treated with DMSO vehicle (−), MK886, and Gue1654 as indicated. Data for all panels are displayed as boxplots (one-way ANOVA with Tukey’s multiple comparisons test; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001). NTEM assays were n=6 biological replicates/group, and eicosanoid analyses were n=4 biological replicates/group; all experiments were repeated on at least two separate occasions.