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VEGF 165 ‐Dependent Switch from Increased Vessel Density to Increased Vessel Diameter and Increased Endothelial NOS Activity
Author(s) -
ParsonsWingerter Patricia,
Chandrasekharan Unni M.,
McKay Terri L.,
Williams Glenn L.,
Vickerman Mary B.,
Farr Andrew G.,
Radhakrishnan Krishnan,
Dicorleto Paul E.
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a708-d
Subject(s) - angiogenesis , chorioallantoic membrane , enos , blood vessel , vascular endothelial growth factor , quail , chemistry , anatomy , neovascularization , nitric oxide synthase , biology , nitric oxide , vegf receptors , medicine , endocrinology
Vascular endothelial growth factor‐165 (VEGF 165 ) regulates numerous cellular activities during angiogenesis, but its complex effects on vascular morphology are not highly quantified. By fractal‐based, multiparametric branching analysis of vascular pattern, maximum increases in vessel density were stimulated at lower VEGF concentrations, but maximum increases in vessel diameter, leakage and activity of endothelial nitric oxide synthase (eNOS) were stimulated at higher VEGF concentrations. Following exogenous application of VEGF 165 to the quail chorioallantoic membrane (CAM) for 24 h at embryonic day 7, vessel density and diameter were measured in arterial endpoints by the fractal dimension (D f ) and generational branching parameters for vessel area density (A v ), vessel length density (L v ) and vessel diameter (D v ) with the computer code VESGEN. The VEGF‐induced switch from normal vessels of increased vessel density to abnormal, dilated vessels characteristic of tumor vasculature and other pathologies resulted from a threefold increase in VEGF concentration (1.25 to 5 μg/CAM). Activity of eNOS increased to 60% after 3 h at 5 μg VEGF/CAM compared to 10% at 1.25μg/CAM, correlating positively with the VEGF‐dependent switch from increased vessel density to increased vessel diameter. Supported by NASA Glenn IRD04‐54 & NCC3‐622/782/912; NSF EEC‐9529161; NIH GM‐40711 & HL29582.

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