Department of Clinical Biochemistry, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Digestive Disease Research Center, Digestive Disease Research Institute, Tehran University of Medical Sciences, Tehran, Iran.
Immun Inflamm Dis. 2024 Mar;12(3):e1224. doi: 10.1002/iid3.1224.
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.
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.
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.
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.
溃疡性结肠炎（UC）是一种由多种因素引起的慢性炎症性肠病，如免疫系统功能障碍和遗传因素。microRNAs（miRNAs）在 UC 的发病机制中起着至关重要的作用，特别是通过 JAK-STAT 途径。我们的目的是研究 miRNA-101 与 JAK2-STAT3 信号通路与 UC 患者炎症细胞因子的关系。
我们招募了 35 名 UC 患者和 35 名健康个体作为对照组，来自伊朗德黑兰 Shariati 医院。根据临床、实验室、组织学和结肠镜检查标准对患者进行诊断。从组织样本中提取 RNA 和蛋白质。实时 PCR 用于评估 miRNA-101、白细胞介素（IL）-1β、IL-6、肿瘤坏死因子（TNF）-α和 IL-10 基因的表达水平，而 Western blot 用于测量 P-STAT3、总 STAT3 和 JAK2 蛋白的水平。
与对照组相比，病例组中促炎细胞因子 TNF-α、IL-1β 和 IL-6 的表达显著增加，而 IL-10 的表达显著降低。此外，UC 患者中 miRNA-101 的表达显著升高。miRNA-101 与 IL-6 表达之间存在显著相关性，表明它们之间的关系及其对细胞信号通路 JAK2-STAT3 的可能影响。磷酸化和总 STAT3 和 JAK2 蛋白表达无显著变化。
本研究提供了 UC 组织中 miRNA-101 表达增加的证据，表明 miRNA-101 与 IL-6 表达之间可能存在相关性，它们可能参与 JAK2-STAT3 途径。该研究证实了 UC 患者促炎细胞因子和抗炎性 IL-10 的改变。然而，需要进一步的研究来全面了解 miRNA-101 在 UC 发病机制中的确切作用。
