Mediators implicated in estrogen production and cellular proliferation in endometriotic lesions and PFCs are inhibited by LXA4 treatment.

Rajesh Kumar (72124), Anne-Catherine Clerc (526757), Ilaria Gori (526758), Ronan Russell (526759), Chiara Pellegrini (526760), Lerisa Govender (526761), Jean-Christophe Wyss (249968), Dela Golshayan (1503082), Geraldine O. Canny (492710)
2015 · doi:10.1371/journal.pone.0089742.g006 · W6941674641
other OA: green CC0
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LXA4 treatment inhibited mRNA expression of estrogen production and proliferation mediators and reduced ERα immunohistochemical staining in mouse endometriotic lesions.

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This study investigated the effects of Lipoxin A4 (LXA4) on de novo and established endometriosis using a mouse model. Researchers analyzed mRNA transcript levels of key mediators involved in estrogen production and cellular proliferation, including CYP19a1, ERα, GREB1, CCND1, and c-Myc, within both endometriotic lesions and pelvic fibroid cysts (PFCs). The results demonstrated that LXA4 treatment significantly inhibited the expression of these genes and reduced ERα protein levels as confirmed by immunohistochemical staining. These findings indicate that LXA4 prevents disease progression by attenuating prostaglandin E2 production and disrupting estrogen signaling pathways. This paper is centrally about endometriosis — specifically the molecular mechanisms underlying lesion progression and the therapeutic potential of LXA4 in inhibiting estrogen-driven cellular proliferation.

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Abstract

mRNA 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.
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Lipoxin A4 Prevents the Progression of De Novo and Established Endometriosis in a Mouse Model by Attenuating Prostaglandin E2 Production and Estrogen Signaling Figure 6 Mediators implicated in estrogen production and cellular proliferation in endometriotic lesions and PFCs are inhibited by LXA4 treatment. mRNA 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.

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endometriosis

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