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Updated: Jun 4, 2026
07:09
Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
Published on: January 7, 2019
Small peptide encoded by MALAT1 aggravates colitis via upregulating GIP expression in enterocyte.
Da Teng1, Bing Ma1, Xinmo Liu1
1Department of General Surgery, the First Medical Centre, Chinese PLA General Hospital, 28 Fuxing Road, Beijing, China.
Biochemical Pharmacology
|June 2, 2026
Summary
Researchers discovered a new peptide, enteroendocrine cells peptide (EECP), that worsens inflammatory bowel disease (IBD) by increasing inflammation. Targeting EECP may offer new treatments for IBD.
Area of Science:
- Gastroenterology
- Molecular Biology
- Immunology
Background:
- Inflammatory bowel disease (IBD) is a chronic intestinal disorder with unclear pathogenic mechanisms.
- Enterocytes and their secreted peptides play a role in IBD, but their specific functions are largely unknown.
Purpose of the Study:
- To identify and characterize novel small peptides involved in IBD pathogenesis.
- To elucidate the mechanistic role of a newly identified peptide in colitis.
Main Methods:
- Identification of a novel peptide (EECP) encoded by MALAT1 in enteroendocrine K cells.
- Analysis of EECP expression in colitis models.
- Investigating the effect of EECP knockout on dextran sulfate sodium-induced colitis.
- Elucidating the molecular mechanism involving EECP, gastric inhibitory polypeptide, and FOXP1.
Main Results:
- EECP expression is upregulated in colitis.
- EECP knockout ameliorates colitis symptoms, reducing immune cell infiltration and intestinal damage.
- EECP promotes gastric inhibitory polypeptide secretion, leading to increased pro-inflammatory cytokine production by macrophages.
- EECP regulates gastric inhibitory polypeptide via interaction with the transcriptional repressor FOXP1.
Conclusions:
- Enterocyte-derived EECP is a key mediator in exacerbating colitis.
- The EECP/gastric inhibitory polypeptide/FOXP1 pathway represents a novel mechanism in IBD pathogenesis.
- EECP presents a potential therapeutic target for inflammatory bowel disease treatment.
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