title: Expression and mitogenic effect of fibroblast growth factor-9 in human endometriotic implant is regulated by aberrant production of estrogen.
abstract: Fibroblast growth factor-9 (FGF-9) is a steroid-regulated mitogen and survival factor for nerve and mesenchymal cells. In the current study, we determined the expression pattern and functional roles of FGF-9 in the ectopic endometriotic lesions. We found that FGF-9 and its receptors were effectively expressed by ectopic endometriotic tissues. The expression of FGF-9 was greater in the early stage of endometriosis, compared with the severe stage, which is consistent with concentration of 17 beta-estradiol in the peritoneal fluid of women with endometriosis. In addition, expression of FGF-9 in ectopic endometriotic stromal cell was inhibited by treatment with ICI 182,870 indicating it is likely regulated by estrogen in an autocrine manner. Administration of 17 beta-estradiol induced FGF-9, FGF receptor 2IIIc, and FGF receptor 3IIIc expression in endometriotic stromal cells. Concordant with this result, treatment of endometriotic stromal cells with 4-hydroxyandrostenedione (an aromatase inhibitor) or ICI 182,870 inhibited their proliferation, and that was reversed by coadministration with 17 beta-estradiol or FGF-9. In conclusion, expression of FGF-9 in endometriotic stromal cells is associated with aberrant production of estrogen. The capability of proliferation possessed by endometriotic stromal cell during menstruation when ovarian 17 beta-estradiol is in the nadir may be mediated, at least in part, by autocrined estrogen-stimulated expression of FGF-9 and its receptors.
authors: Department of Physiology, National Cheng Kung University Medical College, Tainan 701, Taiwan, Republic of China.
authors: Lih-Yuh C
authors: LY
authors: Wing
authors: Pei-Chin
authors: PC
authors: Chuang
authors: Meng-Hsing
authors: MH
authors: Wu
authors: Hsiu-Mei
authors: HM
authors: Chen
authors: Shaw-Jenq
authors: SJ
authors: Tsai
mesh_terms: D002455:Cell Division / Q000187:drug effects; D016889:Endometrial Neoplasms; D004715:Endometriosis / Q000378:metabolism / Q000503:physiopathology*; D004958:Estradiol / Q000096:biosynthesis* / Q000494:pharmacology; D005260:Female; D051525:Fibroblast Growth Factor 9; D005346:Fibroblast Growth Factors / Q000235:genetics* / Q000378:metabolism / Q000494:pharmacology; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D008598:Menstruation / Q000502:physiology; D008934:Mitogens / Q000235:genetics* / Q000378:metabolism / Q000494:pharmacology; D011388:Prolactin / Q000096:biosynthesis; D017468:Receptors, Fibroblast Growth Factor / Q000235:genetics; D017154:Stromal Cells / Q000166:cytology; D014407:Tumor Cells, Cultured
chemical_list: C496459:FGF9 protein, human; D051525:Fibroblast Growth Factor 9; D008934:Mitogens; D017468:Receptors, Fibroblast Growth Factor; D004958:Estradiol; D005346:Fibroblast Growth Factors; D011388:Prolactin