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Isolation of Human Endometrial Stromal Cells for In Vitro Decidualization
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Isolation of Human Endometrial Stromal Cells for In Vitro Decidualization

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Abnormal cell differentiation and p21 expression of endometrial epithelial cells following developmental exposure to

A Yoshida1, R R Newbold, D Dixon

  • 1Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA.

Toxicologic Pathology
|May 11, 2000
PubMed

Insights

Neonatal exposure to diethylstilbestrol (DES) in mice altered endometrial cell differentiation and cell cycle. These changes were linked to modified estrogen receptor alpha (ER alpha) and p21 gene expression, independent of p53.

Area of Science:

  • Endocrinology
  • Developmental Biology
  • Molecular Biology

Background:

  • Neonatal exposure to endocrine-disrupting chemicals can lead to long-term reproductive health issues.
  • Diethylstilbestrol (DES) is a synthetic estrogen with known developmental toxicity.
  • Understanding gene expression changes in response to neonatal DES exposure is crucial for assessing risks.

Purpose of the Study:

  • To investigate the effects of neonatal diethylstilbestrol (DES) exposure on gene expression related to cell differentiation and cell cycle in mouse endometrial epithelial cells.
  • To identify specific molecular mechanisms underlying DES-induced abnormalities in the developing uterus.

Main Methods:

  • Immunohistochemical analysis was performed on mouse uteri from 5 to 22 days of age.
  • Mice received daily subcutaneous injections of DES or corn oil (control) from postnatal days 1-5.
  • Expression levels of estrogen receptor alpha (ER alpha), c-fos, lactoferrin, p21, and p53 proteins were assessed.

Main Results:

  • Neonatal DES exposure enhanced ER alpha and c-fos expression in endometrial epithelial cells at 5-8 days of age.
  • Increased lactoferrin expression, a marker of estrogen exposure, was observed, though it decreased after DES cessation.
  • Frequent p21 protein staining, a mitotic inhibitor, was noted in DES-treated mice (5-15 days), while p53 accumulation was not detected.

Conclusions:

  • Neonatal DES exposure can cause suppressed cell cycle activity and abnormal estrogen-related differentiation in endometrial epithelial cells.
  • Transient alterations in ER alpha expression and p21 gene induction, via a p53-independent pathway, may contribute to these developmental effects.
  • These findings highlight the potential for early-life exposure to endocrine disruptors to impact uterine development and function.

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