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PMID:8605350

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Citation

Barleon, B, Sozzani, S, Zhou, D, Weich, HA, Mantovani, A and Marmé, D (1996) Migration of human monocytes in response to vascular endothelial growth factor (VEGF) is mediated via the VEGF receptor flt-1. Blood 87:3336-43

Abstract

Treatment of human monocytes with vascular endothelial growth factor (VEGF) isolated from tumor cell supernatants was reported to induce monocyte activation and migration. In this study we show that recombinant human VEGF165, and VEGF121 had a maximal effect on human monocyte migration at 65 to 250 pmol/L. Chemotactic activity of VEGF165 was inhibited by a specific antiserum against VEGF, by heat treatment of VEGF165, and by protein kinase inhibitors. In addition, we could show that VEGF-stimulated monocyte migration is mediated by a pertussis toxin-sensitive GTP-binding protein. Placenta growth factor (PlGF152), a heparin-binding growth factor related to VEGF, was also chemotactic for monocytes at concentrations between 2.5 and 25 pmol/L. In accordance with these findings, human monocytes showed specific and saturable binding for 125I-VEGF165 (half-maximal binding at 1 to 1.5 nmol/L). Using Northern blot analysis, we further could show that human monocytes express only the gene for the VEGF receptor type, flt-1, but not for the second known VEGF receptor, KDR. Resting monocytes expressed low levels of flt-1 gene only. Brief exposure (2 to 4 hours) of human monocytes to lipopolysaccharide, a prototypic monocyte activator, led to a significant upregulation of the flt-1 mRNA level. The results presented here suggest that monocyte chemotaxis in response to VEGF and most likely to PlGF152 is mediated by flt-1 and thus show a possible function for the VEGF-receptor flt-1.

Links

PubMed

Keywords

Binding, Competitive; Chemotaxis, Leukocyte/drug effects; Chemotaxis, Leukocyte/physiology; Endothelial Growth Factors/pharmacology; Endothelium, Vascular/cytology; GTP-Binding Proteins/physiology; Humans; Lymphokines/pharmacology; Monocytes/drug effects; Muscle, Smooth/cytology; N-Formylmethionine Leucyl-Phenylalanine/pharmacology; Neutrophils/drug effects; Neutrophils/physiology; Pertussis Toxin; Pregnancy Proteins/chemistry; Pregnancy Proteins/pharmacology; Proto-Oncogene Proteins/drug effects; Proto-Oncogene Proteins/physiology; Receptor Protein-Tyrosine Kinases/drug effects; Receptor Protein-Tyrosine Kinases/physiology; Receptors, Growth Factor/physiology; Receptors, Vascular Endothelial Growth Factor; Recombinant Proteins/pharmacology; Signal Transduction/drug effects; Signal Transduction/physiology; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-1; Vascular Endothelial Growth Factors; Virulence Factors, Bordetella/pharmacology

Significance

Annotations

Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status

HUMAN:VGFR1

enables

GO:0005021: vascular endothelial growth factor-activated receptor activity

ECO:0000314: direct assay evidence used in manual assertion

F

Seeded From UniProt

complete

HUMAN:VGFR1

enables

GO:0036326: VEGF-A-activated receptor activity

ECO:0000314: direct assay evidence used in manual assertion

F

Seeded From UniProt

complete

HUMAN:VGFR1

involved_in

GO:0035924: cellular response to vascular endothelial growth factor stimulus

ECO:0000314: direct assay evidence used in manual assertion

P

Seeded From UniProt

complete

HUMAN:VGFR1

involved_in

GO:0030335: positive regulation of cell migration

ECO:0000314: direct assay evidence used in manual assertion

P

Seeded From UniProt

complete

HUMAN:VGFR1

involved_in

GO:0016477: cell migration

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete

HUMAN:VGFR1

involved_in

GO:0002548: monocyte chemotaxis

ECO:0000314: direct assay evidence used in manual assertion

P

Seeded From UniProt

complete


See also

References

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