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氢化可的松对人输卵管上皮细胞体外模型中紧密连接基因的影响。

The effects of hydrocortisone on tight junction genes in an in vitro model of the human fallopian epithelial cells.

作者信息

Zhaeentan Shahrzad, Amjadi Fatemeh Sadat, Zandie Zahra, Joghataei Mohammad Taghi, Bakhtiyari Mehrdad, Aflatoonian Reza

机构信息

International Campus, Iran University of Medical Science, Tehran, Iran.

Department of Anatomical Science, Iran University of Medical Science, Tehran, Iran.

出版信息

Eur J Obstet Gynecol Reprod Biol. 2018 Oct;229:127-131. doi: 10.1016/j.ejogrb.2018.05.034. Epub 2018 May 23.

DOI:10.1016/j.ejogrb.2018.05.034
PMID:30173088
Abstract

The tight junction between epithelial cells helps making connections in the fallopian tube and contributes to successful fertilization. Breaking the tight junction complex induces various diseases such as the EP. Previous studies have shown that glucocorticoids are effective in repairing and maintaining intercellular tight junctions in epithelial cells of the fallopian tube, although their mechanism is still unknown. This research is a genomic study of hydrocortisone's effect on epithelial cells of the fallopian tube. Using the human fallopian tube, epithelial cell line (OE-E6/E7) was cultured in four concentrations of hydrocortisone (0 nM, 50 nM, 100 nM and 200 nM) for three durations (24 h, 48 h and 72 h). Glucocorticoids are effective on the expression of Zona occluding-1(ZO-1), Claudin 4, Claudin3, Desmoglein and E-cadherin genes involved in the tight junctions of the fallopian tube. The expression of all genes was up-regulated in the concentrations of 100 nM after 48 h treatment, as compared with the control (0 nM). However, their expression was down-regulated significantly after 72 h treatment (P < 0.05). The present study showed that treatment of epithelial cells of the fallopian tube with glucocorticoid increased the expression of genes involved in tight junctions, including claudin-3, claudin-4, E-cadherin, zona occludin-1 and Desmoglein-1. The obtained data suggests that a new mechanism is developed for glucocorticoid induction of tight junctions by increasing the expression of claudin-3, claudin-4, E-cadherin, zona occludin-1 and Desmoglein-1 genes.

摘要

上皮细胞之间的紧密连接有助于输卵管建立连接,并促进成功受精。破坏紧密连接复合物会引发各种疾病,如子宫内膜异位症。以往研究表明,糖皮质激素对修复和维持输卵管上皮细胞间的紧密连接有效,但其机制尚不清楚。本研究是关于氢化可的松对输卵管上皮细胞作用的基因组研究。使用人输卵管上皮细胞系(OE-E6/E7),在四种浓度(0 nM、50 nM、100 nM和200 nM)的氢化可的松中培养三个时长(24小时、48小时和72小时)。糖皮质激素对参与输卵管紧密连接的闭合蛋白1(ZO-1)、闭合蛋白4、闭合蛋白3、桥粒芯糖蛋白和E-钙黏蛋白基因的表达有影响。与对照组(0 nM)相比,在48小时处理后,所有基因在100 nM浓度下表达上调。然而,在72小时处理后,它们的表达显著下调(P<0.05)。本研究表明,用糖皮质激素处理输卵管上皮细胞可增加参与紧密连接的基因的表达,包括闭合蛋白-3、闭合蛋白-4、E-钙黏蛋白、闭合蛋白-1和桥粒芯糖蛋白-1。获得的数据表明,糖皮质激素通过增加闭合蛋白-3、闭合蛋白-4、E-钙黏蛋白、闭合蛋白-1和桥粒芯糖蛋白-1基因的表达,形成了一种诱导紧密连接的新机制。

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