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Long non-coding RNA Mirt2 interacts with long non-coding RNA IFNG-AS1 to regulate ulcerative colitis
Chenyang Li1, Lujia Cui2, Siqiong Li2
1Department of Gastroenterology, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China.
Experimental and Therapeutic Medicine
|September 21, 2020
Summary
Long non-coding RNAs Mirt2 and interferon-γ antisense RNA I (IFNG-AS1) show an inverse relationship in ulcerative colitis (UC). Mirt2 suppresses apoptosis, while IFNG-AS1 promotes it, suggesting their interaction influences UC pathogenesis.
Area of Science:
- Molecular Biology
- Gastroenterology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are crucial in regulating cellular processes.
- Lipopolysaccharide (LPS)-induced inflammation is a key factor in ulcerative colitis (UC) pathogenesis.
- Mirt2 and interferon-γ antisense RNA I (IFNG-AS1) exhibit opposing roles in inflammation.
Purpose of the Study:
- To investigate the interaction between Mirt2 and IFNG-AS1 in ulcerative colitis (UC).
- To evaluate the diagnostic potential of Mirt2 and IFNG-AS1 in UC patients.
Main Methods:
- Quantitative reverse transcription-PCR to measure lncRNA levels in plasma samples.
- Receiver operating characteristic (ROC) curve analysis for diagnostic value assessment.
- Cell apoptosis assays to determine the role of Mirt2 and IFNG-AS1 in colonic epithelial cells.
Main Results:
- Mirt2 was downregulated and IFNG-AS1 was upregulated in UC patients, showing an inverse correlation.
- Altered expression of both lncRNAs effectively distinguished UC patients from healthy controls.
- LPS treatment downregulated Mirt2 and upregulated IFNG-AS1 in colonic cells.
- Mirt2 overexpression decreased, while IFNG-AS1 overexpression increased, colonic epithelial cell apoptosis.
- IFNG-AS1 overexpression partially reversed the protective effects of Mirt2 overexpression.
Conclusions:
- Mirt2 and IFNG-AS1 interact in the context of ulcerative colitis (UC).
- This interaction influences colonic epithelial cell apoptosis, potentially contributing to UC development.
- Mirt2 and IFNG-AS1 serve as potential diagnostic biomarkers for UC.
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