Increased duodenal expression of miR-146a and -155 in pediatric Crohn’s disease

Figure 1 Expression of microRNA-146a (A), microRNA-155 (B) and microRNA-122 (C) in the duodenal mucosa of pediatric patients with Crohn’s disease. Expression of microRNA (miR)-146a was significantly higher in the inflamed duodenal mucosa of children with Crohn’s disease (CD) compared to the intact mucosa and controls. miR-155 showed significantly elevated expression in the inflamed region of the duodenum compared to the control group. There was no significant difference in the expression of miR-122 between the groups. ^aP≤ 0.05 vs Control; ^bP≤ 0.001 vs Control; ^dP≤ 0.01 vs CD intact.

Figure 2 Effect of transforming growth factor-β on the expression of microRNA-146a (A), and microRNA-155 (B) in duodenal epithelial cells. Transforming growth factor (TGF)-β did not have any effect on the expression of microRNA (miR)-146a. TGF-β significantly decreased the expression of miR-155. There was no miR-122 expression detected, ^aP≤ 0.05 vs Control.

Figure 3 Effect of transforming growth factor-β on the expression of microRNA-146a (A), microRNA-155 (B), and microRNA-122 (C) in duodenal fibroblasts. Transforming growth factor (TGF)-β significantly decreased the expression of microRNA (miR)-146a and miR-155. TGF-β had no effect on the expression of miR-122, ^aP≤ 0.05 vs Control, ^bP≤ 0.01 vs Control.

Figure 4 Schematic representation of the target interactions between transforming growth factor-β - microRNA-146a, -155 and -122. Transforming growth factor (TGF)-β is considered to be a major anti-inflammatory cytokine playing an important role in the pathogenesis of inflammatory bowel disease. MicroRNA (miR)-146a, -155 and -122 act as possible regulators of the TGF-β signal transduction, with capacity to induce apoptosis, cell migration, invasion and proliferation. Moreover, TGF-β induces and represses the transcription of various genes. Data shown in the figure are based on MiRTarBase Database. SMAD: Mothers against decapentaplegic homolog; RhoA: Ras homolog gene family, member A.