Journal
JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY
Volume 48, Issue 4, Pages 545-555Publisher
HISTOCHEMICAL SOC INC
DOI: 10.1177/002215540004800412
Keywords
vascular permeability factor (VPF); vascular endothelial growth factor (VEGF); vascular permeability factor receptor (VPFR); vascular endothelial growth factor receptor (VEGFR); fetal liver kinase 1 (Flk-1); kinase insert domain-containing receptor (KDR); ultrastructure; immunocytochemistry; endothelial cells; tumor vessels; mouse kidney; vesiculovacuolar organelle (WO)
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Funding
- NCI NIH HHS [CA74951, CA-50453] Funding Source: Medline
- NIAID NIH HHS [AI-33372] Funding Source: Medline
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Vascular permeability factor/vascular endothelial growth factor (VPF/VEGF) interacts with two high-affinity tyrosine kinase receptors, VEGFR-1 and VEGFR-2, to increase microvascular permeability and induce angiogenesis. Both receptors are selectively expressed by vascular endothelial cells and are strikingly increased in tumor vessels. We used a specific antibody to localize VEGFR-2 (FLK-1. KDR) in microvascular endothelium of normal mouse kidneys and in the microvessels induced by the TA3/St mammary tumor or by infection with an adenoviral vector engineered to express VPF/VEGF. A pre-embedding method was employed at the light and electron microscopic levels using either nanogold or peroxidase as reporters. Equivalent staining was observed on both the luminal and abluminal surfaces of tumor- and adenovirus-induced vascular endothelium, but plasma membranes at interendothelial junctions were spared except at sites connected to vesiculovacuolar organelles (VVOs). VEGFR-2 was also localized to the membranes and stomatal diaphragms of some VVOs. This staining distribution is consistent with a model in which VPF/VEGF increases microvascular permeability by opening VVOs to allow the transendothelial cell passage of plasma and plasma proteins.
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