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Increased duodenal expression of miR-146a and -155 in pediatric Crohn's disease
Dániel Szűcs1, Nóra Judit Béres1, Réka Rokonay1
1Dániel Szűcs, Csaba Bereczki, Department of Pediatrics and Pediatric Health Care Center, University of Szeged, H-6725 Szeged, Hungary.
Insights
microRNA-146a and microRNA-155 show increased expression in pediatric Crohn's disease duodenal tissue, suggesting their role in inflammatory bowel disease. Transforming growth factor-beta influences these microRNAs in intestinal cells.
Area of Science:
- Gastroenterology
- Molecular Biology
- Pediatric Inflammatory Bowel Disease Research
Background:
- Crohn's disease (CD) is a chronic inflammatory bowel disease.
- MicroRNAs (miRs) are implicated in the pathogenesis of inflammatory conditions.
- The role of specific miRs, such as miR-146a, -155, and -122, in pediatric CD duodenal mucosa requires further elucidation.
Purpose of the Study:
- To investigate the expression levels of miR-146a, -155, and -122 in the duodenal mucosa of pediatric Crohn's disease patients.
- To examine the impact of transforming growth factor-beta (TGF-β) on the expression of these miRs in duodenal epithelial and fibroblast cells.
Main Methods:
- Analysis of duodenal biopsies from pediatric CD patients (inflamed and intact mucosa) and controls using real-time PCR.
- In vitro study involving TGF-β treatment of small intestinal epithelial cells (CCL-241) and primary duodenal fibroblasts.
Main Results:
- miR-146a expression was significantly elevated in inflamed duodenal mucosa of CD patients compared to intact mucosa and controls.
- miR-155 expression was significantly increased in inflamed duodenal mucosa compared to controls.
- TGF-β treatment significantly downregulated miR-155 and miR-146a expression in both epithelial and fibroblast cells, but did not affect miR-122.
Conclusions:
- Elevated miR-146a and miR-155 in inflamed duodenal mucosa suggest their involvement in the pathomechanism of pediatric Crohn's disease.
- Transforming growth factor-beta plays a regulatory role in the expression of miR-146a and miR-155, highlighting a potential therapeutic target.
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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