Estrogen reinforces barrier formation and protects against tumor necrosis factor alpha-induced barrier dysfunction in oral epithelial cells.
Estrogen reinforces barrier formation and protects against tumor necrosis factor alpha-induced barrier dysfunction in oral epithelial cells.
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DOI：
10.5051/jpis.2018.48.5.284
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发表时间：
2018-10
影响因子：
1.9
通讯作者：
Choi Y
中科院分区：
文献类型：
--
作者：
Choi YS;Baek K;Choi Y
上皮屏障功能障碍参与牙周炎和口腔扁平苔藓的病理生理过程。雌激素已被证明可以增强肠和食管上皮的物理屏障功能，我们的目的是研究雌二醇（E2）对人口腔上皮细胞单层的物理屏障和紧密连接（TJ）蛋白的调节作用。用E2、雌激素受体（ER）拮抗剂（ICI 182，780）、肿瘤坏死因子α（TNFα）或地塞米松（Dexa）处理在transwell上培养的HOK-16 B细胞单层，然后测量跨上皮电阻（TER）。通过细胞计数试剂盒（CCK）-8测定来测量细胞增殖。共聚焦显微镜观察TJ蛋白表达及核因子（NF）-κB核转位情况。E2处理以剂量依赖性方式增加TER和连接粘附分子（JAM）-A和闭合小带（ZO）-1的水平，而不影响屏障形成期间的细胞增殖。用TNFα处理紧密连接细胞单层可诱导TER和ZO-1水平降低以及NF-κB核转位。这些TNFα诱导的变化被E2抑制，并且这种作用被ICI 182，780联合处理完全逆转。此外，E2和Dexa对上皮屏障功能具有相加作用。E2通过依赖于细胞核ER的TJ蛋白上调来增强口腔上皮细胞的物理屏障。E2对TNFα诱导的上皮屏障损伤的保护作用及其与Dexa的相加作用表明其可能用于治疗涉及上皮屏障功能障碍的口腔炎性疾病。
Epithelial barrier dysfunction is involved in the pathophysiology of periodontitis and oral lichen planus. Estrogens have been shown to enhance the physical barrier function of intestinal and esophageal epithelia, and we aimed to investigate the effect of estradiol (E2) on the regulation of physical barrier and tight junction (TJ) proteins in human oral epithelial cell monolayers. HOK-16B cell monolayers cultured on transwells were treated with E2, an estrogen receptor (ER) antagonist (ICI 182,780), tumor necrosis factor alpha (TNFα), or dexamethasone (Dexa), and the transepithelial electrical resistance (TER) was then measured. Cell proliferation was measured by the cell counting kit (CCK)-8 assay. The levels of TJ proteins and nuclear translocation of nuclear factor (NF)-κB were examined by confocal microscopy. E2 treatment increased the TER and the levels of junctional adhesion molecule (JAM)-A and zonula occludens (ZO)-1 in a dose-dependent manner, without affecting cell proliferation during barrier formation. Treatment of the tight-junctioned cell monolayers with TNFα induced decreases in the TER and the levels of ZO-1 and nuclear translocation of NF-κB. These TNFα-induced changes were inhibited by E2, and this effect was completely reversed by co-treatment with ICI 182,780. Furthermore, E2 and Dexa presented an additive effect on the epithelial barrier function. E2 reinforces the physical barrier of oral epithelial cells through the nuclear ER-dependent upregulation of TJ proteins. The protective effect of E2 on the TNFα-induced impairment of the epithelial barrier and its additive effect with Dexa suggest its potential use to treat oral inflammatory diseases involving epithelial barrier dysfunction.
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影响因子：
3.4
作者：
Capaldo, Christopher T.;Nusrat, Asma
通讯作者：
Nusrat, Asma
DOI：
10.1152/ajpgi.00412.2004
发表时间：
2005-03-01
影响因子：
4.5
作者：
Ma, TY;Boivin, MA;Said, HM
通讯作者：
Said, HM
影响因子：
14.2
作者：
Swindle, Emily J.;Collins, Jane E.;Davies, Donna E.
通讯作者：
Davies, Donna E.
影响因子：
4.4
作者：
Schaefer, TM;Wright, JA;Wira, CR
通讯作者：
Wira, CR
DOI：
10.1006/bbrc.2001.5519
发表时间：
2001-09-07
影响因子：
3.1
作者：
Pelzer, T;Neumann, M;Neyses, L
通讯作者：
Neyses, L