{"paper_id":"c0280fe8-62c7-4052-98f3-2d831aae06a7","body_text":"Lipoxin A4 Prevents the Progression of De Novo and Established Endometriosis in a Mouse Model by Attenuating Prostaglandin E2 Production and Estrogen Signaling\nFigure 6\nMediators implicated in estrogen production and cellular proliferation in endometriotic lesions and PFCs are inhibited by LXA4 treatment.\nmRNA was extracted from endometriotic lesions and PFCs and subjected to qPCR analysis to assess transcript levels of A. CYP19a1, B. ERα, C. GREB1, D. CCND1, E. c-Myc and F. ERα, G. CCND1, H. c-Myc, respectively. Results were normalized to GAPDH. Ten mice were used per group (Sham, Veh-, LXA4-treatment) and sacrificed 21 days after surgical induction of endometriosis. Data are presented as mean ± SEM. (***p<0.001 compared to Veh; ζζζ p<0.001 compared to Sham). I. Immunohistochemical staining for ERα was performed on transverse sections of endometriotic lesions from Veh- (left panel) and LXA4-treated (right panel) mice. The negative control is shown in the inset.","source_license":"CC0","license_restricted":false}