VDR regulates Claudin-15 expression in colonic epithelium. [A] Putative VDRE sites in the Claudin-15 promoter. [B] ChIP assay using quantitative PCR followed by SDS-PAGE electrophoresis showed direct binding of VDR to the Claudin-15 promoter. The assay was verified for a primer of a VDRE site on IkBα as a positive control and a primer for a non-VDRE site of Axin1 as a negative control. [C] SDS-PAGE analysis following the ChIP assay verified the binding of VDR to the Claudin-15 promoter, n = 3–6. [D] A working model of intestinal epithelial VDR in maintaining tight junctions and protecting the host from colitis. In colonic epithelial cells, VDR binds directly to the VDRE region of the Claudin-15 promoter, thus increasing the expression of Claudin-15. Different types of tight junction proteins, including Claudin-15, form tight junctions [TJs] in epithelial cells. Chronic inflammation is known to damage these TJs. However, overexpression of VDR protects against inflammation by enhancing the expression of the tight junction protein Claudin-15. VDR, vitamin D receptor; PCR, polymerase chain reaction.