Kevin Osteen
Last active: 2/19/2015

Developmental exposure of mice to TCDD elicits a similar uterine phenotype in adult animals as observed in women with endometriosis.

Nayyar T, Bruner-Tran KL, Piestrzeniewicz-Ulanska D, Osteen KG
Reprod Toxicol. 2007 23 (3): 326-36

PMID: 17056225 · PMCID: PMC1885235 · DOI:10.1016/j.reprotox.2006.09.007

Whether environmental toxicants impact an individual woman's risk for developing endometriosis remains uncertain. Although the growth of endometrial glands and stroma at extra-uterine sites is associated with retrograde menstruation, our studies suggest that reduced responsiveness to progesterone may increase the invasive capacity of endometrial tissue in women with endometriosis. Interestingly, our recent studies using isolated human endometrial cells in short-term culture suggest that experimental exposure to the environmental contaminant 2,3,7,8-tetracholorodibenzo-p-dioxin (TCDD) can alter the expression of progesterone receptor isotypes. Compared to adult exposure, toxicant exposure during development can exert a significantly greater biological impact, potentially affecting the incidence of endometriosis in adults. To address this possibility, we exposed mice to TCDD at critical developmental time points and subsequently examined uterine progesterone receptor expression and steroid responsive transforming growth factor-beta2 expression in adult animals. We find that the uterine phenotype of toxicant-exposed mice is markedly similarly to the endometrial phenotype of women with endometriosis.

MeSH Terms (24)

Animals Blotting, Western Cytochrome P-450 CYP1A1 Disease Models, Animal Endometriosis Endometrium Environmental Pollutants Estradiol Female Humans Immunohistochemistry Liver Male Mice Mice, Inbred C57BL Organ Culture Techniques Ovariectomy Polychlorinated Dibenzodioxins Pregnancy Progesterone Receptors, Progesterone Sex Factors Transforming Growth Factor beta2 Uterus

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