Ability of ovarian steroids to regulate the expression of the fibroblast growth factor family in fibroblasts derived from uterine endometrium

In: Journal of Biomedical Science · 1996 · vol. 3(4) , pp. 280–285 · doi:10.1007/bf02253708 · PMID:11725109 · W2018536431
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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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Abstract

Uterine endometrial neovascularization during the menstrual cycle is regulated by a basic fibroblast growth factor (FGF) in the endometrium, consisting of endothelial and stromal cells. Acidic FGF (FGF-1), basic FGF (FGF-2) and hst-1 (FGF-4) proteins also possess angiogenic potency in vivo. Therefore, it is important to improve our understanding of the role of stromal cells in FGF supply for endometrial neovascularization. In this study, we determined FGF-1, -2, and -4 mRNA and FGF-2 by reverse transcription-polymerase chain reaction-Southern blot analysis, and enzyme-linked immunosorbent assay, respectively, in fibroblasts derived from uterine endometria as a substitute for stromal cells. Experimental results indicate that estradiol significanlty increases the levels of intracellular and secreted FGF-2 and its mRNA expression in the FGF family in the fibroblasts. Moreover, progesterone reduces the estradiol-induced increase. Therefore, endometrial neovascularization might be partially regulated by stroma-derived FGF-2 under the influence of sex steroids through a paracrine cell-to-cell interaction. Copyright 1996 S. Karger AG, Basel
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Abstract

Uterine endometrial neovascularization during the menstrual cycle is regulated by a basic fibroblast growth factor (FGF) in the endometrium, consisting of endothelial and stromal cells. Acidic FGF (FGF-1), basic FGF (FGF-2) and hst-1 (FGF-4) proteins also possess angiogenic potency in vivo. Therefore, it is important to improve our understanding of the role of stromal cells in FGF supply for endometrial neovascularization. In this study, we determined FGF-1,-2, and -4 mRNA and FGF-2 by reverse transcription-polymerase chain reaction-Southern blot analysis, and enzyme-linked immunosorbent assay, respectively, in fibroblasts derived from uterine endometria as a substitute for stromal cells. Experimental results indicate that estradiol significantly increases the levels of intracellular and secreted FGF-2 and its mRNA expression in the FGF family in the fibroblasts. Moreover, progesterone reduces the estradiol-induced increase. Therefore, endometrial neovascularization might be partially regulated by stroma-derived FGF-2 under the influence of sex steroids through a paracrine cell-to-cell interaction. Similar content being viewed by others

References

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chemicals 4
estradiol progesterone estradiol sex hormone

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