Chen Honglei, Lu Rong, Zhang Yong-Guo, Sun Jun
a Department of Biochemistry , Rush University , Chicago , IL , USA.
b Division of Gastroenterology and Hepatology, Department of Medicine , University of Illinois at Chicago , Chicago , IL , USA.
Tissue Barriers. 2018;6(4):1-13. doi: 10.1080/21688370.2018.1540904. Epub 2018 Nov 8.
Vitamin D deficiency has been linked to various inflammatory diseases in lungs, including pneumonia, asthma and chronic obstructive pulmonary disease. However, the mechanisms by which vitamin D and vitamin D receptor reduce inflammation in lung diseases remain poorly understood. In this study, we investigated the expression and cell-specific distribution of tight and adherens junctions in the lungs of vitamin D receptor-deficient (VDR) mice. Our results demonstrated that mRNA and protein levels of claudin-2, claudin-4 and claudin-12 were significantly decreased in the lungs of VDR mice. Other tight and adherens junction proteins, such as ZO-1, occludin, claudin-10, β-catenin, and VE-cadherin, showed significant differences in expression in the lungs of VDR and wild-type mice. These data suggest that altered expression of tight and adherens junction molecules, especially of claudin-2, -4, -10, -12, and -18, after chronic pneumonia caused by VDR deletion could increase lung permeability.Therefore, VDR may play an important role in maintaining pulmonary barrier integrity. Further studies should confirm whether vitamin D/VDR is beneficial for the prevention or treatment of lung diseases.
维生素D缺乏与肺部的多种炎症性疾病有关，包括肺炎、哮喘和慢性阻塞性肺疾病。然而，维生素D和维生素D受体减轻肺部疾病炎症的机制仍知之甚少。在本研究中，我们调查了维生素D受体缺陷（VDR）小鼠肺部紧密连接和黏附连接的表达及细胞特异性分布。我们的结果表明，VDR小鼠肺部的claudin-2、claudin-4和claudin-12的mRNA和蛋白质水平显著降低。其他紧密连接和黏附连接蛋白，如ZO-1、闭合蛋白、claudin-10、β-连环蛋白和血管内皮钙黏蛋白，在VDR小鼠和野生型小鼠肺部的表达存在显著差异。这些数据表明，VDR缺失导致慢性肺炎后，紧密连接和黏附连接分子，特别是claudin-2、-4、-10、-12和-18的表达改变，可能会增加肺通透性。因此，VDR可能在维持肺屏障完整性方面发挥重要作用。进一步的研究应证实维生素D/VDR对肺部疾病的预防或治疗是否有益。
