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Published on: April 21, 2015
Angiopoietin-2 in experimental colitis.
Vijay C Ganta1, Walter Cromer, Ginny L Mills
1Department of Molecular and Cellular Physiology, Louisiana Health Sciences Centre-Shreveport, Louisiana 71130-3932, USA.
Inflammatory Bowel Diseases
|November 11, 2009
Summary
Angiopoietin-2 (Ang-2) drives inflammation and blood vessel changes in inflammatory bowel disease (IBD). Mice lacking Ang-2 show reduced gut inflammation and improved protein loss, suggesting Ang-2 as a therapeutic target.
Area of Science:
- Gastroenterology
- Immunology
- Vascular Biology
Background:
- Inflammatory bowel disease (IBD) involves leukocyte infiltration, vascular remodeling, and protein loss.
- The specific role of angiopoietin-2 (Ang-2) in IBD pathogenesis, including inflammation initiation and angiogenesis, remains unclear.
Purpose of the Study:
- To investigate the role of Ang-2 in experimental colitis, focusing on its impact on inflammation, leukocyte infiltration, and vascular changes.
Main Methods:
- Experimental colitis was induced in wild-type (WT) and Ang-2 knockout (Ang-2(-/-)) mice.
- Disease activity, histopathology, leukocyte infiltration, and vascular density were assessed.
- Assays included myeloperoxidase, immunohistochemistry, and SDS-PAGE.
Main Results:
- Ang-2(-/-) mice exhibited significantly attenuated leukocyte infiltration, inflammation, and blood/lymphatic vessel density compared to WT mice.
- Gut capillary fragility and water loss were increased earlier in Ang-2(-/-) mice.
- Reduced colon length and less severe gut histopathology were observed in Ang-2(-/-) mice, with improved protein-losing enteropathy.
Conclusions:
- Ang-2 mediates inflammatory hemangiogenesis, lymphangiogenesis, and neutrophil infiltration in DSS colitis.
- While Ang-2 contributes to IBD features, its absence partially alleviates clinical manifestations.
- These findings highlight Ang-2 as a potential therapeutic target for IBD and other inflammatory conditions.
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