[HTML][HTML] Increased duodenal expression of miR-146a and-155 in pediatric Crohn's disease

D Szűcs, NJ Béres, R Rokonay, K Boros… - World journal of …, 2016 - ncbi.nlm.nih.gov
D Szűcs, NJ Béres, R Rokonay, K Boros, K Borka, Z Kiss, A Arató, AJ Szabó, Á Vannay
World journal of gastroenterology, 2016ncbi.nlm.nih.gov
AIM: To evaluate the role of microRNA (miR)-146a,-155 and-122 in the duodenal mucosa of
pediatric patients with Crohn's disease (CD) and the effect of transforming growth factor-β
(TGF-β) on these miRs in duodenal epithelial and fibroblast cells. METHODS: Formalin-
fixed, paraffin-embedded biopsies derived from the macroscopically inflamed (CD inflamed:
n= 10) and intact (CD intact: n= 10) duodenal mucosa of pediatric CD patients and control
children (C: n= 10) were examined. Expression of miR-146a,-155 and-122 was determined …
Abstract
AIM: To evaluate the role of microRNA (miR)-146a,-155 and-122 in the duodenal mucosa of pediatric patients with Crohn’s disease (CD) and the effect of transforming growth factor-β (TGF-β) on these miRs in duodenal epithelial and fibroblast cells.
METHODS: Formalin-fixed, paraffin-embedded biopsies derived from the macroscopically inflamed (CD inflamed: n= 10) and intact (CD intact: n= 10) duodenal mucosa of pediatric CD patients and control children (C: n= 10) were examined. Expression of miR-146a,-155 and-122 was determined by real-time polymerase-chain reaction (PCR). The expression of the above miRs was investigated in recombinant human TGF-β (1 nmol/L, 24 h) or vehicle treated small intestinal epithelial cells (CCL-241) and primary duodenal fibroblast cells derived from healthy children as well.
RESULTS: Expression of miR-146a was significantly higher in the inflamed duodenal mucosa compared to the intact duodenal mucosa of children with CD (CD inflamed: 3.21±0.50 vs CD intact: 0.62±0.26, P≤ 0.01) and to the control group (CD inflamed: 3.21±0.50 vs C: 1.00±0.33, P≤ 0.05). The expression of miR-155 was significantly increased in the inflamed region of the duodenum compared to the control group (CD inflamed: 4.87±1.02 vs Control: 1.00±0.40, P≤ 0.001). The expression of miR-122 was unchanged in the inflamed or intact mucosa of CD patients compared to controls. TGF-β treatment significantly decreased the expression of miR-155 in small intestinal epithelial cells (TGF-β: 0.7±0.083 vs Control: 1±0.09, P≤ 0.05) and also the expression of miR-146a (TGF-β: 0.67±0.04 vs Control: 1±0.15, P≤ 0.01) and miR-155 (TGF-β: 0.72±0.09 vs Control: 1±0.06, P≤ 0.05) in primary duodenal fibroblasts compared to corresponding vehicle treated controls. TGF-β treatment did not influence the expression of miR-122.
CONCLUSION: The elevated expression of miR-146a and-155 in the inflamed duodenal mucosa of CD patients suggests the role of these miRs in the pathomechanism of inflammatory bowel disease. Anti-inflammatory TGF-β plays an important role in the regulation of the expression of these miRs.
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