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Inflammatory Bowel Disease I: Ulcerative Colitis01:27

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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...
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The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the...
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Chronic bowel diseases are a group of long-term conditions affecting the digestive tract, characterized by inflammation and damage to the gut lining. These conditions primarily include irritable bowel syndrome and inflammatory bowel disease.
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The gastric glands contain parietal cells that secrete hydrochloric acid (HCl) for digestion. The cells secrete HCl because it is highly corrosive and essential for breaking down food. To achieve this, they secrete hydrogen and chloride ions into the lumen of the gastric glands, which combine to form HCl.
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Long Noncoding RNA FBXL19-AS1-Mediated Ulcerative Colitis-Associated Intestinal Epithelial Barrier Defect.

Xun Zhao1, De-Jun Cui2, Liu-Chan Yang2

  • 1Department of Gastroenterology, Guizhou Provincial People's Hospital, Medical College of Guizhou University, No. 83, East Zhongshan Road, Guiyang City, 550002, Guizhou Province, China. zxun025@outlook.com.

Tissue Engineering and Regenerative Medicine
|September 1, 2022
PubMed
Summary
This summary is machine-generated.

Long non-coding RNA FBXL19 antisense RNA 1 (FBXL19-AS1) exacerbates ulcerative colitis (UC) by reducing miR-339-3p, which targets RHOB. Inhibiting FBXL19-AS1 ameliorates UC in a mouse model.

Keywords:
Intestinal epithelial barrier defectLong noncoding RNA FBXL19-AS1RAS homologous protein BUlcerative colitismicroRNA-339-3p

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Area of Science:

  • Gastroenterology
  • Molecular Biology
  • RNA Biology

Background:

  • Ulcerative colitis (UC) is a chronic inflammatory bowel disease.
  • The role of long non-coding RNAs (lncRNAs) in UC pathogenesis is increasingly recognized.
  • FBXL19 antisense RNA 1 (FBXL19-AS1) is a lncRNA whose function in UC remains unclear.

Purpose of the Study:

  • To investigate the role of FBXL19-AS1 in the development of ulcerative colitis (UC).
  • To elucidate the underlying molecular mechanism of FBXL19-AS1 in UC.
  • To explore the potential of targeting FBXL19-AS1 for UC treatment.

Main Methods:

  • FBXL19-AS1 expression analysis in UC patients and a dextran sodium sulfate (DSS)-induced mouse colitis model.
  • Assessment of colonic histopathology, apoptosis, fibrosis, and intestinal permeability in mice.
  • Enzyme-linked immunosorbent assay (ELISA) for inflammatory cytokines (IL-1β, IL-18).
  • RNA immunoprecipitation and dual luciferase reporter assays to confirm molecular interactions.

Main Results:

  • FBXL19-AS1 expression was significantly upregulated in DSS-induced colitis.
  • FBXL19-AS1 interference or miR-339-3p overexpression attenuated colonic inflammation, apoptosis, and barrier defects in mice.
  • FBXL19-AS1 acts as a sponge for miR-339-3p, and miR-339-3p targets RHOB.
  • RHOB overexpression counteracted the protective effects of FBXL19-AS1 inhibition.

Conclusions:

  • FBXL19-AS1 promotes UC development by sponging miR-339-3p, thereby relieving RHOB inhibition.
  • FBXL19-AS1 aggravates intestinal epithelial barrier defects in DSS-induced colitis.
  • Targeting FBXL19-AS1 may represent a therapeutic strategy for ulcerative colitis.