Vitamin D Receptor Deletion Leads to the Destruction of Tight and Adherens Junctions in Lungs

• Published in: Tissue barriers 2018-10, Vol.6 (4), p.1-13
• Main Authors: Chen, Honglei, Lu, Rong, Zhang, Yong-Guo, Sun, Jun
• Format: Article
• Language: English
• Subjects: Adherens Junctions - metabolism; Adherens Junctions - pathology; Animals; Capillary Permeability - physiology; Female; Lung - metabolism; Lung - pathology; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Receptors, Calcitriol - metabolism; Research Paper; Tight Junctions - metabolism; Tight Junctions - pathology; Vitamin D Deficiency - complications; Vitamin D Deficiency - metabolism; Vitamin D Deficiency - physiopathology
• ISSN: 2168-8370; 2168-8362; 2168-8370
• DOI: 10.1080/21688370.2018.1540904

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.