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ABIN1 Inhibits Inflammation through Necroptosis-Dependent Pathway in Ulcerative Colitis
Jing Bao1, Bin Ye1, Yuhan Ren1
1Department of Gastroenterology, Shengzhou People's Hospital, Shaoxing, China.
Genetics Research
|August 29, 2022
Summary
ABIN1, a protein involved in inflammation, is upregulated in ulcerative colitis (UC). Overexpressing ABIN1 inhibits necroptosis and reduces inflammation, suggesting ABIN1 activation as a potential therapy for UC.
Area of Science:
- Gastroenterology
- Immunology
- Cell Biology
Background:
- Ulcerative colitis (UC) involves chronic intestinal inflammation and epithelial injury.
- Intestinal barrier dysfunction is a key feature throughout UC development.
- ABIN1, an ubiquitin-binding protein, influences tissue homeostasis and autoimmunity, but its role in UC is unclear.
Purpose of the Study:
- To investigate the role of ABIN1 in ulcerative colitis (UC) pathogenesis.
- To determine the relationship between ABIN1 expression and necroptosis in UC.
- To explore ABIN1's potential as a therapeutic target for UC.
Main Methods:
- Assessed mRNA and protein levels of ABIN1 and necroptosis markers (RIPK1, RIPK3, MLKL) in human UC samples.
- Utilized a dextran sodium sulfate (DSS)-induced mouse model of colitis.
- Performed in vitro gain and loss function assays of ABIN1 in CACO-2 cells.
Main Results:
- ABIN1, RIPK1, RIPK3, and MLKL were upregulated in UC patients and DSS-induced colitis models.
- Overexpression of ABIN1 inhibited necroptosis and reduced pro-inflammatory cytokines (IL1B, IL6, IL8, TNF-α) in intestinal epithelial cells.
- Blocking RIPK1 alleviated colitis and cell death, mirroring the effects of ABIN1 overexpression.
Conclusions:
- ABIN1 dysregulation is linked to uncontrolled necroptosis and inflammation in UC.
- ABIN1 negatively regulates UC occurrence and progression.
- ABIN1 activation presents a potential therapeutic strategy for ulcerative colitis.
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