Estrogenicity of bisphenol A in a human endometrial carcinoma cell line

Bergeron, Renée; Thompson, Tommy B.; Leonard, Linda S.; Pluta, Linda; Gaido, Kevin W.

doi:10.1016/s0303-7207(98)00202-0

Cited by 74 publications

(33 citation statements)

References 37 publications

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“…For these studies, we used the human uterine epithelial cell line ECC-1 that expresses a functional progesterone receptor and estrogen receptor (ER)␣. ER␤ is also expressed by ECC-1 cells but to insignificant levels (37)(38)(39)(40). Using ECC-1 cells, we examined the mRNA expression and secretion of HBD2 and CXCL8 following stimulation of these cells with IL-1␤ in the presence of sex hormones.…”

Section: Il-1␤-mediated Proinflammatory Responsesmentioning

confidence: 99%

IL-1β-Mediated Proinflammatory Responses Are Inhibited by Estradiol via Down-Regulation of IL-1 Receptor Type I in Uterine Epithelial Cells

Schaefer

Wright

Pioli

et al. 2005

The Journal of Immunology

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The objective of this study was to examine the effects of sex hormones on IL-1β-mediated responses by uterine epithelial cells. The mRNA expression and secretion of human β-defensin-2 and CXCL8 by uterine epithelial cells was examined following stimulation with IL-1β in the presence of estradiol or progesterone. Estradiol inhibited the IL-1β-mediated mRNA expression and secretion of human β-defensin-2 and CXCL8 by uterine epithelial cells while progesterone had no effect. Inhibition of the IL-1β-mediated response by estradiol was dose dependent, with maximal inhibition observed using 10−7 to 10−10 M, and was shown to be mediated through the estrogen receptor because addition of a pure estrogen receptor antagonist abrogated this effect. The mechanism by which estradiol inhibits IL-1β-mediated responses by uterine epithelial cells appears to be the down-modulation of the IL-1R type I, thereby reducing the uterine epithelial cell’s ability to respond to IL-1β. These results suggest that the inhibitory effect of estradiol on IL-1β-mediated inflammatory responses by uterine epithelial cells indicates a link between the endocrine and immune systems and may be crucial for dampening proinflammatory responses during the time of ovulation or pregnancy.

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Section: Il-1␤-mediated Proinflammatory Responsesmentioning

confidence: 99%

IL-1β-Mediated Proinflammatory Responses Are Inhibited by Estradiol via Down-Regulation of IL-1 Receptor Type I in Uterine Epithelial Cells

Schaefer

Wright

Pioli

et al. 2005

The Journal of Immunology

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show abstract

“…In fact 20 -30 g of BPA/ml was detected in the saliva of patients who had been treated with a dental sealant (Olea et al, 1996). BPA is said to exert a weak estrogenic activity both in vitro and vivo (Krishnan et al, 1993;Steinmetz et al, 1997;Gould et al, 1998;Ashby and Tinwell, 1998;Bergeron et al, 1999;Schafer et al, 1999;Papaconstantinou et al, 2000). Compared with 17 -estradiol (E2), the effect of BPA as an estrogen is 1,000 -15,000 times lower (Gaido et al, 1997;Nagel et al, 1997;Steinmetz et al, 1997;Milligan et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Adverse effects of bisphenol A to spermiogenesis in mice and rats

Toyama

Suzuki-Toyota

Maekawa

et al. 2004

Archives of Histology and Cytology

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“…Such binding is functional, since exposure to BPA can result in uterine changes in female rats at sufficiently high oral doses, or at lower doses when administered parenterally (Morrissey et al, 1987;Laws et al, 2000). Unlike 17␤-estradiol, this interaction does not affect cell proliferation in the human endometrial cell line, ECC-1 (Gould et al, 1998;Bergeron et al, 1999). However, BPA can cause estrogen-mediated effects at high doses, and low-dose effects have been reported (vom Saal et al, 1997).…”

mentioning

confidence: 99%