Endometriosis Knowledgebase


A repository for genes associated with endometriosis

Results


PMID 26453052
Gene Name USF2
Condition Endometriosis
Association Associated
Population size 86
Population details 86(37 women undergoing diagnostic laparoscopy for endometriosis associated with pain and/or infertility, 49 women without endometriosis undergoing laparoscopy for tubal ligation or hysterectomy for a benign non-endometrial gynecologic condition (controls)
Age Endometriosis grp: 33.9 ± 5.6 years, Control grp: 36.7 ± 6.5 years
Sex Female
Infertility type Female infertility
Associated genes USF2a, ER, GPER and USF2b
Other associated phenotypes Endometriosis
Differential expression of upstream stimulatory factor (USF) 2 variants in eutopic endometria from women with endometriosis: estradiol regulation.

Biol Res. 2015 Oct 9;48:56. doi: 10.1186/s40659-015-0047-2.

Castro, Jazmin| Araya, German| Inostroza, Pamela| Hidalgo, Paulina| Gonzalez-Ramos, Reinaldo| Sovino, Hugo| Boric, M Angelica| Fuentes, Ariel| Johnson, M Cecilia

Faculty of Medicine, Institute of Maternal and Child Research, University of Chile, P.O. Box 226-3, Santiago, Chile. jazmin.castro@gmail.com.| Faculty of Medicine, Institute of Maternal and Child Research, University of Chile, P.O. Box 226-3, Santiago,

BACKGROUND: Endometriosis, 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. RESULTS: Upstream 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 ERalpha) 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. CONCLUSION: These data strongly suggest that USF2 variants and P450Arom are regulated by E2 through ERalpha 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.

Mesh Terms: Adult| Aromatase/*metabolism| Biopsy| Endometriosis/*metabolism/pathology/physiopathology| Endometrium/cytology/*metabolism| Epithelial Cells/secretion| Estradiol/*metabolism| Female| Gene Expression/*genetics| Humans| Immunoblotting| Menstrual