A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä

Functional Expression of FSH Receptor in Endometriotic Lesions




TekijätPonikwicka-Tyszko D, Chrusciel M, Stelmaszewska J, Bernaczyk P, Sztachelska M, Sidorkiewicz I, Doroszko M, Tomaszewski J, Tapanainen JS, Huhtaniemi I, Wolczynski S, Rahman NA

KustantajaENDOCRINE SOC

Julkaisuvuosi2016

JournalJournal of Clinical Endocrinology and Metabolism

Tietokannassa oleva lehden nimiJOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM

Lehden akronyymiJ CLIN ENDOCR METAB

Vuosikerta101

Numero7

Aloitussivu2905

Lopetussivu2914

Sivujen määrä10

ISSN0021-972X

eISSN1945-7197

DOIhttps://doi.org/10.1210/jc.2016-1014


Tiivistelmä
Context: FSH receptor (FSHR), besides being expressed in gonads, is also expressed in some extragonadal tissues at low levels.Objective: We examined the functional expression of FSHR in different types of endometriotic lesions.Design: Extensive studieswerecarried out to detect functional FSHR expression and FSH-stimulated estrogen production in ovarian endometriomas and recto-vaginal endometriotic nodules (RVEN). Normal endometrium, ovary, and myometrium tissues from nonpregnant cycling women served as controls.Settings: This laboratory-based study was carried out on tissue specimens from patients with endometriosis and healthy donors.Results: Endometriotic lesions and normal secretory-phase endometrium showed FSHR expression at both mRNA and protein level. RVEN and ovarian endometrioma demonstrated up-regulated CYP19A1, dependent on the activation of CYP19A1 proximal promoter II. Estrogen receptor-beta (ESR2) expression was significantly increased in RVEN vs normal endometrium. Recombinant human FSH stimulation of RVEN explants significantly increased estradiol production and CYP19A1 and ESR2 expression. FSHR was up-regulated in recombinant human FSH-stimulated endometrial and decidualized stromal cells with increased CYP19A1 expression.Conclusions: We described a novel functional FSHR expression, where FSH-stimulated CYP19A1 expression and estrogen production in RVEN are demonstrated. This locally FSH-induced estrogen production may contribute to the pathology, development, progression, and severity of RVEN.



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