Journal article
Vascular endothelial growth factor regulation of Weibel-Palade—body exocytosis
Blood, Vol.105(1), pp.207-214
01/01/2005
DOI: 10.1182/blood-2004-04-1519
PMCID: PMC2705620
PMID: 15345585
Abstract
Vascular endothelial growth factor (VEGF) not only regulates angiogenesis, vascular permeability, and vasodilation but also promotes vascular inflammation. However, the molecular basis for the proinflammatory effects of VEGF is not understood. We now show that VEGF activates endothelial cell exocytosis of Weibel-Palade bodies, releasing vasoactive substances capable of causing vascular thrombosis and inflammation. VEGF triggers endothelial exocytosis in part through calcium and phospholipase C-γ (PLC-γ) signal transduction. However, VEGF also modulates endothelial cell exocytosis by activating endothelial nitric oxide synthase (eNOS) production of nitric oxide (NO), which nitrosylates Nethylmaleimide sensitive factor (NSF) and inhibits exocytosis. Thus, VEGF plays a dual role in regulating endothelial exocytosis, triggering pathways that both promote and inhibit endothelial exocytosis. Regulation of endothelial exocytosis may explain part of the proinflammatory effects of VEGF.
Details
- Title: Subtitle
- Vascular endothelial growth factor regulation of Weibel-Palade—body exocytosis
- Creators
- Kenji Matsushita - Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD; the Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD; and the Department of Comparative Medicine, The Johns Hopkins University School of Medicine, Baltimore, MDMunekazu Yamakuchi - Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD; the Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD; and the Department of Comparative Medicine, The Johns Hopkins University School of Medicine, Baltimore, MDCraig N Morrell - Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD; the Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD; and the Department of Comparative Medicine, The Johns Hopkins University School of Medicine, Baltimore, MDMichitaka Ozaki - Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD; the Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD; and the Department of Comparative Medicine, The Johns Hopkins University School of Medicine, Baltimore, MDBrian O'Rourke - Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD; the Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD; and the Department of Comparative Medicine, The Johns Hopkins University School of Medicine, Baltimore, MDKaikobad Irani - Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD; the Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD; and the Department of Comparative Medicine, The Johns Hopkins University School of Medicine, Baltimore, MDCharles J Lowenstein - Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD; the Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD; and the Department of Comparative Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD
- Resource Type
- Journal article
- Publication Details
- Blood, Vol.105(1), pp.207-214
- DOI
- 10.1182/blood-2004-04-1519
- PMID
- 15345585
- PMCID
- PMC2705620
- ISSN
- 0006-4971
- eISSN
- 1528-0020
- Language
- English
- Date published
- 01/01/2005
- Academic Unit
- Cardiovascular Medicine; Radiation Oncology; Fraternal Order of Eagles Diabetes Research Center; Internal Medicine
- Record Identifier
- 9984047714702771
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