Expression and mitogenic effect of fibroblast growth factor-9 in human endometriotic implant is regulated by aberrant production of estrogen

Lih‐Yuh C. Wing, Wing LY, Lih-Yuh C. Wing, Chuang PC, Pei-Chin Chuang, Wu MH, Meng-Hsing Wu, Meng‐Hsing Wu, Hsiu‐Mei Chen, Hsiu-Mei Chen, Chen HM, Shaw-Jenq Tsai, Shaw‐Jenq Tsai
The Journal of clinical endocrinology and metabolism · 2003 · vol. 88(11) , pp. 5547–5554 · doi:10.1210/jc.2003-030597 · PMID:14602803 · W2031607357
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Fibroblast growth factor-9 expression in human endometriotic implants is increased by estrogen and contributes to stromal cell proliferation, particularly when peritoneal estrogen levels are high.

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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.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Estradiol Fibroblast Growth Factors Mitogens Cell Division Cell Division Cell Division Endometrial Neoplasms Endometrial Neoplasms Endometriosis Endometriosis Endometriosis Estradiol Estradiol Estradiol Female Female Fibroblast Growth Factor 9 Fibroblast Growth Factor 9 Fibroblast Growth Factors

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Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

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