Differential expression of upstream stimulatory factor USF 2 variants in eutopic endometria from women with endometriosis: estradiol regulationReportar como inadecuado

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Biological Research

, 48:56

First Online: 09 October 2015Received: 01 September 2015Accepted: 30 September 2015DOI: 10.1186-s40659-015-0047-2

Cite this article as: Castro, J., Araya, G., Inostroza, P. et al. Biol Res 2015 48: 56. doi:10.1186-s40659-015-0047-2


BackgroundEndometriosis, pro-inflammatory and invasive benign disease estrogen dependent, abnormally express in endometria the enzyme P450Arom, positively regulated by steroid factor-1 SF-1. Our objective was to study the nuclear protein contents of upstream stimulating factor 2 USF2a and USF2b, a positive regulator of SF-1, throughout the menstrual cycle in eutopic endometria from women with and without control endometriosis and the involvement of nuclear estrogen receptors ER and G-coupled protein estrogen receptor GPER-1.

ResultsUpstream stimulating factor 2 protein contents were higher in mid USF2b and late USF2a and USF2b secretory phase in eutopic endometria from endometriosis than control p < 0.05. In isolated control epithelial cells incubated with E2 and PGE2, to resemble the endometriosis condition, the data showed: a significant increase of USF2a and USF2b nuclear protein contents when treated with E2, PPT specific agonist for ERα or G1 specific agonist for GPER1; b no increase in USF2 binding to SF-1 E-Box-DNA consensus sequence in E2-treated cells; c USF2 variants protein contents were not modified by PGE2; d SF-1 nuclear protein content was significantly higher than basal when treated with PGE2, E2 or G1, stimulation unaffected by ICI nuclear ER antagonist; and e increased p < 0.05 cytosolic protein contents of P450Arom when treated with PGE2, E2, PPT or G1 compared to basal, effect that was additive with E2 + PGE2 together. Nevertheless, in endometriosis cells, the high USF2, SF-1 and P450Arom protein contents in basal condition were unmodified.

ConclusionThese data strongly suggest that USF2 variants and P450Arom are regulated by E2 through ERα and GPER1, whereas SF-1 through GPER1, visualized by the response of the cells obtained from control endometria, being unaffected the endogenously stimulated cells from endometriosis origin. The lack of E2 stimulation on USF2-SF-1 E-Box-DNA-sequence binding and the absence of PGE2 effect on USF2 variants opposite to the strong induction that they exert on SF1 and P450 proteins suggest different mechanisms and indirect regulations. The sustained USF2 variants protein expression during the secretory phase in eutopic endometria from women with endometriosis may participate in the pathophysiology of this disease strongly associated with infertility and its characteristic endometrial invasion to ectopic sites in the pelvic cavity.

KeywordsUSF2 GPER1 Endometriosis Eutopic endometrium Estrogen receptor Estrogen receptor specific agonists SF-1 P450Arom AbbreviationsUSF2upstream stimulatory factor

SF-1steroid factor-1

GPER1G-coupled protein estrogen receptor 1

P450Aromaromatase enzyme



ICI 182,7807α,17β-94,4,5,5,5-Pentafluoropentylsulfinylnonylestra-1,3,510-triene-3,17-diol



PGE2prostaglandin E2

ERestrogen receptor

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Fuente: https://link.springer.com/

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