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Updated: Mar 29, 2026

Perturbations of Circulating miRNAs in Irritable Bowel Syndrome Detected Using a Multiplexed High-throughput Gene Expression Platform
10:37

Perturbations of Circulating miRNAs in Irritable Bowel Syndrome Detected Using a Multiplexed High-throughput Gene Expression Platform

Published on: November 30, 2016

8.8K

MicroRNA-24 inhibits serotonin reuptake transporter expression and aggravates irritable bowel syndrome

Xiu-Jun Liao1, Wei-Ming Mao1, Qin Wang1

  • 1Department of Colorectal Surgery, Hangzhou Third Hospital, Hangzhou, 310009, People's Republic of China.

Biochemical and Biophysical Research Communications
|December 4, 2015
PubMed

Insights

MicroRNAs (miRNAs) like miR-24 are implicated in irritable bowel syndrome (IBS) pathogenesis. Targeting miR-24 may alleviate IBS symptoms by regulating serotonin reuptake transporter (SERT) expression.

Area of Science:

  • Gastroenterology
  • Molecular Biology
  • MicroRNA Research

Background:

  • Irritable bowel syndrome (IBS) is a prevalent functional gastrointestinal disorder.
  • MicroRNAs (miRNAs) are key regulators in physiological and pathological processes.
  • The specific role of miR-24 in IBS pathogenesis requires further elucidation.

Purpose of the Study:

  • To investigate the role of miR-24 in the pathogenesis of IBS.
  • To explore the underlying mechanism involving serotonin reuptake transporter (SERT).

Main Methods:

  • Analysis of miR-24 and SERT expression in human IBS colon tissues and an IBS mouse model.
  • Utilized Real-time PCR and western blot for expression analysis.
  • Employed luciferase reporter assay to identify SERT as a miR-24 target.
  • Assessed the effect of miR-24 inhibition on pain thresholds and MPO activity in IBS mice.

Main Results:

  • miR-24 expression was significantly upregulated in intestinal mucosa of IBS patients and mice.
  • SERT was identified as a direct target gene of miR-24.
  • Inhibition of miR-24 increased pain thresholds and reduced colonic inflammation in IBS mice.
  • miR-24 inhibition led to increased SERT mRNA and protein levels in intestinal cells.

Conclusions:

  • miR-24 contributes to IBS pathogenesis.
  • The mechanism involves the regulation of SERT expression by miR-24.
  • Targeting miR-24 presents a potential therapeutic strategy for IBS.
Keywords:
Irritable bowel syndromeMouse modelSERTmiR-24

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