Ability of ovarian steroids to regulate the expression of the fibroblast growth factor family in fibroblasts derived from uterine endometrium
Journal of Biomedical Science, ISSN: 1423-0127, Vol: 3, Issue: 4, Page: 280-285
1996
- 5Citations
- 2Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations5
- Citation Indexes5
- CrossRef4
- Captures2
- Readers2
Article Description
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.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0029833972&origin=inward; http://dx.doi.org/10.1007/bf02253708; http://www.ncbi.nlm.nih.gov/pubmed/11725109; http://www.springerlink.com/index/10.1007/BF02253708; http://www.springerlink.com/index/pdf/10.1007/BF02253708; http://link.springer.com/10.1007/BF02253708; https://link.springer.com/article/10.1007%2FBF02253708; https://dx.doi.org/10.1007/bf02253708; https://link.springer.com/article/10.1007/BF02253708
Springer Nature
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