Yuki Takuo, Haratake Akinori, Koishikawa Hisa, Morita Kazumasa, Miyachi Yoshiki, Inoue Shintaro
Basic Research Laboratory, Kanebo Cosmetics Inc., Kanagawa, Japan.
Exp Dermatol. 2007 Apr;16(4):324-30. doi: 10.1111/j.1600-0625.2006.00539.x.
Recent research suggests that tight junctions (TJs) are located in the stratum granulosum, where they contribute to the barrier function of the epidermis. In this study, we investigated the formation of functional TJs in cultured normal human epidermal keratinocytes. We observed the development of permeability barrier function through the process of Ca(2+)-induced differentiation. Immunofluorescence analyses at 96 h after Ca(2+)-induced differentiation revealed concentrated portions of occludin, a TJ-specific marker, arranged as continuous lines circumscribing individual flattened suprabasal cells in areas with high concentrations of claudin-1 and -4. Transient Ca(2+) depletion reversibly disrupted the continuous network of TJ proteins and the permeability barrier. We also found that the addition of ochratoxin A weakened the permeability barrier and the expression of claudin-4. Our findings suggest that TJ proteins contribute to the permeability barrier in epidermal keratinocytes.
近期研究表明，紧密连接（TJs）位于颗粒层，在那里它们对表皮的屏障功能有贡献。在本研究中，我们调查了培养的正常人表皮角质形成细胞中功能性紧密连接的形成。我们通过Ca(2+)诱导分化的过程观察到了渗透屏障功能的发展。Ca(2+)诱导分化96小时后的免疫荧光分析显示，封闭蛋白（一种紧密连接特异性标志物）的浓缩部分排列成连续的线条，在紧密连接蛋白-1和-4浓度高的区域围绕着单个扁平的基底上层细胞。短暂的Ca(2+)耗竭可逆地破坏了紧密连接蛋白的连续网络和渗透屏障。我们还发现，添加赭曲霉毒素A会削弱渗透屏障和紧密连接蛋白-4的表达。我们的研究结果表明，紧密连接蛋白有助于表皮角质形成细胞中的渗透屏障。
