Fig. 2: VDR induces miR-26a/b by binding with VDRE in HOKs.
From: MicroRNA-26a/b have protective roles in oral lichen planus
a Schematic illustration of VDR binding sites in the promoter regions of miR-26a/b genes. b ChIP analysis showing the increases of miR-26a/b levels after 36-hour VDR plasmids transfection in HOKs, bar indicates log2 fold change, n = 3. qPCR analysis of miR26-a/b expression in HOKs challenged by activated CD4+ T cells (c) or LPS (d) with or without VDR plasmids, n = 3. Differential expression of miR-26a/b in oral keratinocytes of VDRKO (e), paricalcitol-treated (f), or vitamin D-deficient (g) mice, n = 5. Paricalcitol is an analog of vitamin D. h Correlation of fold change in OLP biopsies between VDR and miR-26a/b (r = 0.85081, P = 0.00036, Spearman’s correlation test for miR-26a; r = 0.79941, P = 0.02852, Spearman’s correlation test for miR-26b), n = 14. i Correlation between 25(OH)D concentrations and miR-26a/b levels in serum from OLP patient (r = 0.44655, P = 2.86 × 10−11, Spearman’s correlation test for miR-26a; r = 0.58412, P = 2.87 × 10-11, Spearman’s correlation test for miR-26b), n = 14. *P < 0.05, **P < 0.01, ***P < 0.001 vs. corresponding control. Ctrl control, VDRKO VDR knockout, Pari paricalcitol, VD-D vitamin D deficiency.
