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Methods for Studying Uterine Contributions to Pregnancy Establishment in an Ovariectomized Mouse Model
Published on: April 7, 2023
Progesterone maintains amniotic tight junctions during midpregnancy in mice
Ken Kobayashi1, Hideki Miwa, Masato Yasui
1Department of Pharmacology, School of Medicine, Keio University, Tokyo, Japan. kkobaya@anim.agr.hokudai.ac.jp
Molecular and Cellular Endocrinology
|February 5, 2011
Summary
Progesterone maintains tight junctions (TJs) in the amniotic epithelium during midpregnancy. Blocking progesterone receptors with RU-486 increased amniotic membrane permeability and altered TJ protein expression.
Area of Science:
- Reproductive biology
- Epithelial biology
- Developmental biology
Background:
- The amniotic epithelium forms a barrier regulating fluid flux via tight junctions (TJs).
- Progesterone influences TJs in other epithelial tissues, but its role in the amniotic epithelium is unclear.
Purpose of the Study:
- To investigate the influence of progesterone on amniotic epithelial TJs.
- To determine the role of the progesterone receptor (PR) pathway in maintaining amniotic TJs.
Main Methods:
- Administration of RU-486 (a PR antagonist) to pregnant mice.
- Organ culture of amniotic membranes with varying progesterone concentrations.
- Immunohistochemistry and permeability assays to assess TJ integrity and protein expression.
Main Results:
- RU-486 treatment disrupted claudin-3 and claudin-4 localization and expression, increasing amniotic membrane permeability.
- Progesterone increased claudin-3 and claudin-4 expression in a dose-dependent manner in organ cultures.
- Progesterone receptors (PRs) were present in midpregnancy but absent in late pregnancy amniotic epithelium.
Conclusions:
- The progesterone/PR pathway is crucial for maintaining TJs in the amniotic epithelium during midpregnancy.
- Progesterone positively regulates TJ components, likely via PRs, to control amniotic barrier function.
