MicroRNA-142-5p facilitates the pathogenesis of ulcerative colitis by regulating SOCS1

Jing Han1,2, Yawei Li3, Hong Zhang1

  • 1Department of Gastroenterology, The East Branch of The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology Shijiazhuang, China.

Abstract

Insights

MicroRNA (miR)-142-5p is upregulated in ulcerative colitis (UC) and worsens intestinal inflammation by downregulating SOCS1, increasing IL-6 and IL-8. This suggests miR-142-5p as a potential therapeutic target for UC.

Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Immunology

Background:

  • Abnormal microRNA (miRNA) levels are linked to ulcerative colitis (UC).
  • MicroRNA (miR)-142-5p is notably upregulated in UC patients.
  • The specific role of miR-142-5p in UC pathogenesis requires elucidation.

Purpose of the Study:

  • To investigate the role of miR-142-5p in the context of ulcerative colitis (UC).
  • To determine the relationship between miR-142-5p and suppressor of cytokine signaling 1 (SOCS1) in UC.
  • To assess the impact of miR-142-5p and SOCS1 on inflammatory cytokine production in UC.

Main Methods:

  • miRNA microarray and quantitative RT-PCR were used to analyze miRNA expression in UC patients and controls.
  • The regulatory interaction between miR-142-5p and SOCS1 was assessed using luciferase reporter assays.
  • Levels of IL-6 and IL-8 were measured to evaluate the functional roles of miR-142-5p and SOCS1 in UC progression.

Main Results:

  • miR-142-5p expression was significantly upregulated in UC patients and inversely correlated with SOCS1 expression.
  • miR-142-5p directly targets the 3'-UTR of SOCS1, inhibiting its expression.
  • miR-142-5p influences the secretion of IL-6 and IL-8, and SOCS1 dysfunction reverses these effects.

Conclusions:

  • miR-142-5p exacerbates intestinal inflammation in active UC by downregulating SOCS1.
  • This downregulation leads to increased secretion of pro-inflammatory cytokines IL-6 and IL-8.
  • Targeting miR-142-5p may offer a therapeutic strategy for managing ulcerative colitis.

Related Concept Videos

MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
3.6K
MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After...
23.8K
Cystic Fibrosis: Pathogenesis01:23

Cystic Fibrosis: Pathogenesis

Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body.
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation,...
661
Inflammatory Bowel Disease I: Ulcerative Colitis01:27

Inflammatory Bowel Disease I: Ulcerative Colitis

Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
795
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
1.8K
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
1.1K