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Absence of placental growth factor blocks dextran sodium sulfate-induced colonic mucosal angiogenesis, increases mucosal hypoxia and aggravates acute colonic injury.

Lab Invest.. 2010-04;  90(4):566-76
Hindryckx P, Waeytens A, Laukens D, Peeters H, Van Huysse J, Ferdinande L, Carmeliet P, De Vos M. 1Department of Gastroenterology, Ghent University, Gent, Belgium; 2Department of Pathology, Ghent University, Gent, Belgium; 3Vesalius Research Center, VIB, Leuven, Belgium; 4Vesalius Research Center, KU Leuven, Leuven, Belgium
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摘要

Angiogenesis has recently been described as a component of inflammatory bowel disease. Placental growth factor (PlGF), a vascular endothelial growth factor (VEGF) homologue, establishes its angiogenic capacity under pathophysiological conditions. We investigated the function of PlGF in experimental models of acute colitis. Acute colonic damage was induced in PlGF knock-out ((-/-)) mice and PlGF wild-type ((+/+)) mice by dextran sodium sulfate (DSS) and trinitrobenzenesulfonic acid (TNBS). The concentrations of PlGF and VEGF were measured in distal colonic lysates using an enzyme-linked immunosorbent assay. Colonic injury was evaluated by assessing colon length, colonocyte apoptosis (by terminal dUTP nick-end la... More

关键词

angiogenesis; experimental colitis; inflammatory bowel disease; intestinal mucosal hypoxia; placental growth factor; vascular endothelial growth factor