1997
DOI: 10.1074/jbc.272.27.17097
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Vasoactive Peptides Modulate Vascular Endothelial Cell Growth Factor Production and Endothelial Cell Proliferation and Invasion

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Cited by 177 publications
(125 citation statements)
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“…TSH downregulates ANP receptor number (Tseng et al 1991) in human thyroid cells but there are no data on the regulation of ANP expression. In endothelial cells, both ANP and ET-1 regulate VEGF synthesis, ANP being inhibitory whereas ET-1 is stimulatory (Pedram et al 1997). In this way, these vasoactive peptides can effect a close regulation of endothelial cell proliferation and invasion.…”
Section: ) and Frtl-5 Cells (Vainiomentioning
confidence: 99%
“…TSH downregulates ANP receptor number (Tseng et al 1991) in human thyroid cells but there are no data on the regulation of ANP expression. In endothelial cells, both ANP and ET-1 regulate VEGF synthesis, ANP being inhibitory whereas ET-1 is stimulatory (Pedram et al 1997). In this way, these vasoactive peptides can effect a close regulation of endothelial cell proliferation and invasion.…”
Section: ) and Frtl-5 Cells (Vainiomentioning
confidence: 99%
“…Furthermore, ET-1 potentiates the effect of several proangiogenic factors in vitro, including PDGF and VEGF (Pedram et al, 1997;Yang et al, 1999). ET-1 also stimulates invasion and morphological differentiation of human umbilical vein endothelial cells (HUVEC) in matrigel in vitro, and this may be facilitated via ET-1-induced production of matrix metalloproteinase-2 (MMP-2) by endothelial cells (Salani et al, 2000b).…”
Section: Endothelin and Angiogenesismentioning
confidence: 99%
“…ET-1 is a potent mitogen for both endothelial cells and vascular smooth muscle cells (VSMC) in vitro (Komuro et al, 1988;Pedram et al, 1997). In addition, ET-1 may indirectly enhance endothelial cell proliferation through stimulation of vascular endothelial growth factor (VEGF) production by other cell types (Pedram et al, 1997;Salani et al, 2000a).…”
Section: Endothelin and Angiogenesismentioning
confidence: 99%
“…With respect to ET receptors, predominantly ET A R mediates tumour-associated functions, whereas there is less evidence for ET B R-dependent tumour-related functions (Grant et al, 2003;Nelson et al, 2003). Engagement of ET A -receptor by ET-1 triggers tumorigenesis and tumour progression by activation of tumour proliferation, invasion, angiogenesis, and inhibition of apoptosis (Pedram et al, 1997;Bagnato and Catt, 1998;Bagnato et al, 1999;Eberl et al, 2000b;Salani et al, 2000;Rosano et al, 2001;Del Bufalo et al, 2002). There is also evidence for an autocrine and/or paracrine mechanism of action of ET-1 including angiogenesis-promoting effects in malignant tissues.…”
mentioning
confidence: 99%