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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
Summary
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.
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.
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