ArticleDigestive diseases and sciences1999
Vascular endothelial growth factor (VEGF) in Crohn's disease: increased production by peripheral blood mononuclear cells and decreased VEGF165 labeling of peripheral CD14+ monocytes.
Article in Digestive diseases and sciences, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 31 citations in OpenAlex.
- A zebrafish model of inflammatory lymphangiogenesis.Biology open · 2015Article
- Characterization of Serum Cytokine Profile in Predominantly Colonic Inflammatory Bowel Disease to Delineate Ulcerative and Crohn's Colitides.Clinical medicine insights. Gastroenterology · 2015Article
- VEGF₁₆₄ isoform specific regulation of T-cell-dependent experimental colitis in mice.Inflammatory bowel diseases · 2011Article
- Up-regulation of intestinal vascular endothelial growth factor by Afa/Dr diffusely adhering Escherichia coli.PloS one · 2007Article
- Elevated levels of vascular endothelial growth factor in serum of patients with D+ HUS.Pediatric nephrology (Berlin, Germany) · 2004Article
- Vascular permeability factor/vascular endothelial growth factor induces lymphangiogenesis as well as angiogenesis.The Journal of experimental medicine · 2002Article
- Vascular endothelial growth factor, endostatin levels and clinical features among patients with ulcerative colitis and irritable bowel syndrome and among healthy controls: a cross-sectional analytical study.Sao Paulo medical journal = Revista paulista de medicinaArticle
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5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Recently, increased serum levels of vascular endothelial growth factor (VEGF) have been shown in patients with inflammatory bowel disease. The origins of the circulating VEGF are still not described. Monocytes play an important role in the inflammatory process. VEGF binding to monocytes mediates monocyte recruitment and activation. The present study investigates the VEGF production of peripheral blood mononuclear cells and the ability of peripheral monocytes to bind VEGF165 in patients with Crohn's disease. Nineteen patients with Crohn's disease and 10 healthy volunteers were studied. VEGF165 labeling of CD14+ monocytes was measured using two-color flow cytometry. Density of VEGF labeling was expressed as the mean fluorescence intensity (MFI). Furthermore, VEGF levels were determined in culture supernatants of unstimulated peripheral blood mononuclear cells. VEGF in culture supernatants was measured using a solid-phase enzyme-linked immunosorbent assay. There was a significantly decreased VEGF165 labeling of monocytes of patients with active Crohn's disease (MFI: 369.9+/-121.6, N = 7, P < 0.002) compared to patients with inactive disease (MFI: 457.7+/-74.5, N = 6) and healthy controls (MFI: 542.9+/-96.2, N = 10). Unstimulated peripheral blood mononuclear cells of patients with active Crohn's disease produced significantly higher amounts of VEGF (1142.6+/-483.9 pg/ml, N = 12, P < 0.001) compared with peripheral blood mononuclear cells of healthy volunteers (113.4+/-101.8 pg/ml, N = 10). VEGF production by peripheral blood mononuclear cells of patients with active disease was significantly increased compared to patients with quiescent disease (261.6+/-254.8 pg/ml, N = 7, P < 0.001). In conclusion, our data describe peripheral blood mononuclear cells as one of the origins of the elevated VEGF serum levels in patients with active Crohn's disease. Furthermore, a decrease in VEGF165 binding sites on peripheral monocytes of patients with active Crohn's disease has been shown. The study underlines the important role of VEGF in Crohn's disease.
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