Ability of ovarian steroids to regulate the expression of the fibroblast growth factor family in fibroblasts derived from uterine endometrium
Estradiol increased FGF-2 and its mRNA in uterine fibroblasts, while progesterone reduced this effect, suggesting steroid regulation of stromal FGF-2 in endometrial neovascularization.
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This study examined how ovarian steroid hormones regulate fibroblast growth factor (FGF) family gene expression in fibroblasts derived from human uterine endometrium, using RT-PCR/Southern blotting to measure FGF-1, FGF-2, and FGF-4 mRNA and ELISA to quantify FGF-2 protein. The authors found that estradiol significantly increased intracellular and secreted FGF-2 levels as well as FGF-family mRNA expression, while progesterone reduced the estradiol-induced increase. A key caveat is that the work uses endometrial-derived fibroblasts as a surrogate for stromal cells rather than studying intact tissue architecture and cell–cell interactions directly. Relevance to endometriosis: the paper focuses on endometrial (and stromal/fibroblast) regulation of angiogenic FGFs by sex steroids, which are mechanistically relevant to endometriosis-associated angiogenesis, though it does not explicitly study endometriosis or adenomyosis in this text.
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