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Roles of Ang‐2 KO in Experimental IBD
Author(s) -
Alexander Jonathan Steven,
Jennings Merilyn H,
Daley Sarah,
Bernas Michael,
Witte Marlys,
Mathis J Michael,
Jordan Paul A,
Wang Yuping
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.764.2
Subject(s) - lymphatic system , inflammatory bowel disease , colitis , infiltration (hvac) , myeloperoxidase , medicine , knockout mouse , lymphatic vessel , endocrinology , inflammation , angiopoietin receptor , pathology , disease , receptor , physics , cancer , thermodynamics , metastasis
Angiopoietin‐2 (Ang‐2) is known to influence blood and lymphatic vessel remodeling, but how Ang‐2 gene knockout influences experimental inflammatory bowel disease (IBD) is not known. We used Ang‐2 gene knockout and control mice in the 3% dextran sulfate model of IBD to investigate how the lack of Ang‐2 affects vascular remodeling and indices of disease activity (over 7d). Ang‐2 +/+ and ‐/‐ mice showed equivalent levels of disease activity (stool blood, form and wasting) and weight loss was similar in both groups. There was a signficant increase in both blood (MECA‐32+) and lymphatic (VEGFR‐3+) vessel densities in colitic (DSS‐treated) groups (p<0.05). These increases were significantly reduced in Ang‐2 KO mice, and were also accompanied by decreased concentrations of gut neutrophils (myeloperoxidase activity). Colitic inflamed Ang‐2 ‐/‐ gut tissue show evidence of dysplastic MECA32+/VEGFR3+ networks which were not observed in non‐colitic Ang‐2 KO's. Histopathological scores in DSS colitis were partially, but not completely, resolved by Ang‐2 gene deficiency, and suggest that Ang‐2 plays complex roles in the initiation of IBD possibly by controlling tissue remodeling and leukocyte infiltration of tissues.