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Investigating the association between the tissue expression of miRNA-101, JAK2/STAT3 with TNF-α, IL-6, IL-1β, and IL-10 cytokines in the ulcerative colitis patients. | LitMetric

AI Article Synopsis

  • Ulcerative colitis (UC) is a chronic inflammatory disease linked to immune dysfunction and genetics, where microRNAs like miRNA-101 are believed to influence the disease through the JAK-STAT signaling pathway.
  • A study with 35 UC patients and 35 healthy controls found increased levels of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and decreased IL-10 in UC patients, along with a higher expression of miRNA-101.
  • The findings suggest a potential connection between miRNA-101 and IL-6 in UC, indicating their role in the JAK2-STAT3 pathway, although more research is needed to clarify miRNA-101's exact function in

Article Abstract

Background: Ulcerative colitis (UC) is a chronic inflammatory bowel disease caused by numerous factors, such as immune system dysfunction and genetic factors. MicroRNAs (miRNAs) play a crucial role in UC pathogenesis, particularly via the JAK-STAT pathway. Our aim was to investigate the association between miRNA-101 and JAK2-STAT3 signaling pathway with inflammatory cytokines in UC patients.

Methods: We enrolled 35 UC patients and 35 healthy individuals as the control group, referred to Shariati Hospital, Tehran, Iran. Patients were diagnosed based on clinical, laboratory, histological, and colonoscopy criteria. RNA and protein extracted from tissue samples. Real-time PCR was used to assess the expression levels of miRNA-101, interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and IL-10 genes, while western blot was employed to measure levels of P-STAT3, total STAT3, and JAK2 proteins.

Results: Expression of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 significantly increased, while the expression of IL-10 significantly decreased in the case group versus controls. Additionally, miRNA-101 expression was significantly higher in UC patients. A significant correlation between miRNA-101 and IL-6 expression was observed, indicating their relationship and possible impact on cell signaling pathways, JAK2-STAT3. No significant changes were observed in phosphorylated and total STAT3 and JAK2 protein expression.

Conclusion: This study provides evidence of increased miRNA-101 expression in UC tissue, suggesting a potential correlation between miRNA-101 and IL-6 expression and their involvement in the JAK2-STAT3 pathway. The study confirms alterations in UC patients' pro-inflammatory cytokines and anti-inflammatory IL-10. However, further investigations are needed to understand the exact role of miRNA-101 in UC pathogenesis fully.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10958669PMC
http://dx.doi.org/10.1002/iid3.1224DOI Listing

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