LXA4 Suppresses Cell Signaling, p38 MAPK and ERK Phosphorylation Induced by Estrogen in ESCs

Another in vitro effect elicited by LXA4 in ESCs is reducing E2-induced p38 MAPK and ERK phosphorylation. Important, estradiol is known to stimulate the activity of these enzymes. Additionally, E2-induced p38 MAPK phosphorylation is significantly reduced in cells treated with E2 and LXA4, suggesting that LXA4 may inhibit endometriosis development by this route, probably through ERs [31]. Further, the inhibition of E2 induced p38 MAPK and ERK phosphorylation is mediated by the FPR2/ALX in vitro [7]. In a proteomic analysis, the combined treatment with E2 and LXA4 resulted in reduced regulated proteins, with LXA4 mediating a suppressive effect on E2-mediated inflammatory cell signaling [33].
