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Thrombospondin and VEGF-R: Is There a Correlation in Inflammatory Bowel Disease?
Author(s) -
Jarosław Wejman,
Michał Pyźlak,
Dariusz Szukiewicz,
Dorota Jarosz,
Wiesław Tarnowski,
Grzegorz Szewczyk
Publication year - 2013
Publication title -
mediators of inflammation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.37
H-Index - 97
eISSN - 1466-1861
pISSN - 0962-9351
DOI - 10.1155/2013/908259
Subject(s) - ulcerative colitis , inflammatory bowel disease , medicine , vascular endothelial growth factor , thrombospondin 1 , biopsy , gastroenterology , colectomy , thrombospondin , crohn's disease , pathology , disease , vegf receptors , angiogenesis , metalloproteinase , matrix metalloproteinase
Up to date several authors discussed interactions between cells forming inflammatory infiltrates in the course of inflammatory bowel disease (IBD), mainly dealing with endoscopic biopsy specimens. These usually contain only mucosa. We have evaluated full bowel wall sections, which seems to be especially important in patients with Crohn's disease (CD). The purpose of our study was to evaluate the relationship between vascular density and expression of thrombospondin-1 (TSP-1) and vascular endothelial growth factor receptor 1 (VEGFR-1) in full-thickness tissue fragments of intestinal wall taken from patients after colectomy, comparing those with IBD to non-IBD control group. Histological sections were immunostained with antibodies against CD-31, TSP-1, and VEGFR-1 and analyzed by pathologists with the use of computer-assisted morphometrics. Our research showed significantly higher vascular density and vascular area percentage in all layers of bowel wall in patients with CD when compared to control. We have also demonstrated differences in vascular density distribution between ulcerative colitis (CU) and CD and between CU and control. However we have not found statistically significant correlation between those findings and VEGFR-1 or TSP-1 expression. Our results might suggest existence of different, TSP-1 independent pathways of antiangiogenesis in IBD.

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