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MiR-32-5p aggravates intestinal epithelial cell injury in pediatric enteritis induced by Helicobacter pylori
Jing Feng1, Jian Guo2, Jun-Ping Wang3
1Institute of Loess Plateau, Shanxi University, Taiyuan 030006, Shanxi Province, China.
Insights
Aberrant miR-32-5p expression is increased in pediatric enteritis caused by Helicobacter pylori (H. pylori) infection. This microRNA promotes intestinal cell death and inflammation via the TAK1-p38 pathway, targeting SMAD6.
Area of Science:
- Gastroenterology
- Molecular Biology
- Microbiology
Background:
- Pediatric enteritis, a common digestive issue in children, can be caused by Helicobacter pylori (H. pylori) infection.
- MicroRNAs (miRNAs) show altered expression in H. pylori-related gastrointestinal diseases.
- A significant increase in miR-32-5p was observed in H. pylori-induced pediatric enteritis, but its role remained unclear.
Purpose of the Study:
- To elucidate the function of dysregulated miR-32-5p in pediatric enteritis associated with H. pylori.
- To investigate the molecular mechanisms underlying miR-32-5p's role in H. pylori infection of intestinal cells.
Main Methods:
- Quantitative real-time polymerase chain reaction (qRT-PCR) to measure miR-32-5p expression.
- Cell Counting Kit-8 assay and flow cytometry to assess cell viability and apoptosis.
- Bioinformatic prediction (TargetScanHuman) and luciferase assays to identify miR-32-5p targets.
- Molecular biology techniques to explore downstream signaling pathways.
Main Results:
- miR-32-5p was significantly upregulated in the serum of children with H. pylori-induced enteritis.
- H. pylori infection increased intestinal epithelial cell apoptosis and miR-32-5p levels.
- Overexpression of miR-32-5p exacerbated apoptosis and inflammatory cytokine release.
- SMAD6 was identified as a direct target of miR-32-5p, and its overexpression partially mitigated H. pylori-induced cell damage.
- The miR-32-5p/SMAD6 axis was found to mediate H. pylori-induced apoptosis via the TAK1-p38 pathway.
Conclusions:
- Aberrant miR-32-5p expression plays a critical role in H. pylori-related pediatric enteritis.
- The TAK1-p38 signaling pathway is implicated in the pathogenesis of H. pylori-induced enteritis involving miR-32-5p.
Background:
Pediatric enteritis is one of the infectious diseases in the digestive system that causes a variety of digestive problems, including diarrhea, vomiting, and bellyache in children. Clinically, Helicobacter pylori (H. pylori) infection is one of the common factors to cause pediatric enteritis. It has been demonstrated that aberrant expression of microRNAs (miRNAs) is found in gastrointestinal diseases caused by H. pylori, and we discovered a significant increase of miR-32-5p in H. pylori-related pediatric enteritis. However, the exact role of miR-32-5p in it is still unknown.
Aim:
To investigate the role of aberrant miR-32-5p in pediatric enteritis induced by H. pylori.
Methods:
MiR-32-5p expression was detected by quantitative real time-polymerase chain reaction. The biological role of miR-32-5p in H. pylori-treated intestinal epithelial cells was evaluated by Cell Counting Kit-8 assay and flow cytometry. The potential target of miR-32-5p was predicted with TargetScanHuman and verified by luciferase assay. The downstream mechanism of miR-32-5p was explored by using molecular biology methods.
Results:
We found that miR-32-5p was overexpressed in serum of H. pylori-induced pediatric enteritis. Further investigation revealed that H. pylori infection promoted the death of intestinal epithelial cells, and increased miR-32-5p expression. Moreover, miR-32-5p mimic further facilitated apoptosis and inflammatory cytokine secretion of intestinal epithelial cells. Further exploration revealed that SMAD family member 6 (SMAD6) was the direct target of miR-32-5p, and SMAD6 overexpression partially rescued cell damage induced by H. pylori. The following experiments showed that miR-32-5p/SMAD6 participated in the apoptosis of intestinal epithelial cells induced by transforming growth factor-β-activated kinase 1 (TAK1)-p38 activation under H. pylori infection.
Conclusion:
Our work uncovered the crucial role of aberrant expression of miR-32-5p in H. pylori-related pediatric enteritis, and suggested that the TAK1-p38 pathway is involved in it.
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