Related Experiment Video
Updated: Jun 27, 2026
Murine Colitis Modeling using Dextran Sulfate Sodium DSS
Published on: January 19, 2010
VDUP1 Deficiency Promotes the Severity of DSS-Induced Colitis in Mice by Inducing Macrophage Infiltration
Ki Hwan Park1, Hyunju Lee1, Hyoung-Chin Kim1
1Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology, 30 Yeongudanji, Cheongwon, Cheongju 28116, Republic of Korea.
Abstract:
The loss of vitamin D3 upregulated protein 1 (VDUP1) has been implicated in the pathogenesis of various inflammation-related diseases. Notably, reduced expression of VDUP1 has been observed in clinical specimens of ulcerative colitis (UC). However, the role of VDUP1 deficiency in colitis remains unclear. In this study, we investigated the role of VDUP1 in dextran sulfate sodium (DSS)-induced experimental colitis in mice. VDUP1-deficient mice were more susceptible to DSS-induced colitis than their wild-type (WT) littermates after 2% DSS administration. VDUP1-deficient mice exhibited an increased disease activity index (DAI) and histological scores, as well as significant colonic goblet cell loss and an increase in apoptotic cells. These changes were accompanied by a significant decrease in MUC2 mRNA expression and a marked increase in proinflammatory cytokines and chemokines within damaged tissues. Furthermore, phosphorylated NF-κB p65 expression was significantly upregulated in damaged tissues in the context of VDUP1 deficiency. VDUP1 deficiency also led to significant infiltration of macrophages into the site of ulceration. An in vitro chemotaxis assay confirmed that VDUP1 deficiency enhanced bone marrow-derived macrophage (BMDM) chemotaxis induced by CCL2. Overall, this study highlights VDUP1 as a regulator of UC pathogenesis and a potential target for the future development of therapeutic strategies.
Insights
Vitamin D3 upregulated protein 1 (VDUP1) deficiency exacerbates experimental colitis by increasing inflammation and tissue damage. Loss of VDUP1 promotes macrophage infiltration and susceptibility to inflammatory bowel disease.
Area of Science:
- Immunology
- Gastroenterology
- Molecular Biology
Background:
- Vitamin D3 upregulated protein 1 (VDUP1) loss is linked to inflammation-related diseases.
- Reduced VDUP1 expression is observed in ulcerative colitis (UC) patients.
- The specific role of VDUP1 deficiency in colitis pathogenesis is not well understood.
Purpose of the Study:
- To investigate the function of VDUP1 in dextran sulfate sodium (DSS)-induced experimental colitis.
- To elucidate the mechanisms by which VDUP1 deficiency impacts colitis severity and molecular responses.
Main Methods:
- Utilized VDUP1-deficient and wild-type (WT) mice in a DSS-induced colitis model.
- Assessed disease activity index (DAI), histological scores, and colonic tissue parameters.
- Measured MUC2 mRNA, proinflammatory cytokines/chemokines, and phosphorylated NF-κB p65 expression.
- Performed in vitro chemotaxis assays using bone marrow-derived macrophages (BMDM) and CCL2.
Main Results:
- VDUP1-deficient mice showed increased susceptibility to DSS-induced colitis with higher DAI and histological scores.
- VDUP1 deficiency resulted in goblet cell loss, increased apoptosis, decreased MUC2 mRNA, and elevated proinflammatory mediators.
- Upregulated phosphorylated NF-κB p65 and enhanced macrophage infiltration were observed in VDUP1-deficient colons.
- In vitro studies confirmed that VDUP1 deficiency enhances CCL2-induced BMDM chemotaxis.
Conclusions:
- VDUP1 plays a protective role in experimental colitis.
- VDUP1 deficiency exacerbates colitis by promoting inflammation, MUC2 reduction, and macrophage recruitment.
- VDUP1 is a potential therapeutic target for ulcerative colitis and other inflammatory bowel diseases.
Related Concept Videos
01:20Inflammatory Bowel Disease II: Ulcerative Colitis
01:25Inflammatory Bowel Disease III: Crohn's Disease