Department of Pharmacology, School of Medicine, Keio University, Tokyo, Japan.
Mol Cell Endocrinol. 2011 Apr 30;337(1-2):36-42. doi: 10.1016/j.mce.2011.01.019. Epub 2011 Feb 1.
The amniotic epithelium is in direct contact with the amniotic fluid and restricts fluid flux via the paracellular pathway by means of tight junctions (TJs). Several factors affect TJs to modulate the paracellular flux. Progesterone contributes to the antenatal formation and disappearance of TJs in uterine and mammary epithelial tissues. In this study, we investigated whether progesterone positively or negatively influences amniotic TJs. The administration of RU-486, a progesterone receptor (PR) antagonist, into pregnant mice adversely affects the localization and expression of claudin-3 and claudin-4 in the amniotic epithelium. RU-486 administration also increased the permeability of the amniotic membrane. In organ-cultured amniotic membranes, progesterone induced increases in claudin-3 and claudin-4 expression in a dose-dependent manner but did not influence their localization. PRs were also present in the amniotic epithelium during midpregnancy but they disappeared during late pregnancy. These results indicate that the progesterone/PR pathway maintains TJs in the amniotic epithelium during midpregnancy.
羊膜上皮与羊水直接接触，并通过紧密连接（TJ）限制细胞旁途径的液体流动。有几种因素会影响 TJ 来调节细胞旁通量。孕激素有助于子宫和乳腺上皮组织中 TJ 的产前形成和消失。在这项研究中，我们研究了孕激素是否对羊膜 TJ 有积极或消极的影响。将孕激素受体（PR）拮抗剂 RU-486 给予怀孕小鼠会对羊膜上皮中 Claudin-3 和 Claudin-4 的定位和表达产生不利影响。RU-486 的给药还增加了羊膜的通透性。在器官培养的羊膜中，孕激素以剂量依赖性方式诱导 Claudin-3 和 Claudin-4 的表达增加，但不影响其定位。PR 也存在于妊娠中期的羊膜上皮中，但在妊娠晚期消失。这些结果表明，孕激素/PR 途径在妊娠中期维持羊膜上皮中的 TJ。
