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Zhu, Wen Hui; Nicosia, Roberto F.

doi:10.1023/a:1021509004829

Cited by 65 publications

(17 citation statements)

References 21 publications

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“…Endothelial cells were specifically highlighted by the endothelial marker Griffonia I-B4 [9], whereas pericytes were positive for α-smooth muscle actin (fig. 4).…”

Section: Resultsmentioning

confidence: 99%

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A New ex vivo Model to Study Venous Angiogenesis and Arterio-Venous Anastomosis Formation

et al. 2005

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Explants of rat inferior vena cava embedded in collagen gel and cultured under serum-free conditions produced microvascular outgrowths composed of endothelial cells and pericytes. Exogenous vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) dose-dependently stimulated angiogenesis and induced the formation of complex networks of highly branched microvessels. VEGF and the VEGF/bFGF combination also promoted pericyte recruitment. Medium conditioned by untreated vena cava cultures contained endogenous VEGF, and a blocking antibody against VEGF significantly reduced the spontaneous angiogenic response of the explants. Vena cava explants exhibited a greater capacity to form neovessels than aortic rings when tested in parallel cultures from the same animal. When compared with aorta-derived microvessels, neovessels of vena cava origin were longer and had fewer pericytes. Vena cava-aorta cocultures produced extensive anastomosing networks of microvessels, which were primarily contributed by the venous explants. Because of its florid angiogenesis and exquisite sensitivity to angiogenic factor stimulation, the vena cava model may provide novel insights into the regulation of the angiogenic process, which typically initiates from the venous side of the vascular bed. Combined with the aortic ring model, this new assay may also enhance our understanding of the mechanisms of anastomosis formation between the arterial and the venous circulations.

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“…Endothelial cells were specifically highlighted by the endothelial marker Griffonia I-B4 [9], whereas pericytes were positive for α-smooth muscle actin (fig. 4).…”

Section: Resultsmentioning

confidence: 99%

“…Explants of inferior vena cava and aortic rings were embedded individually or together in collagen gel using the thin prep modification of the rat aortic ring assay [9]. Collagen was prepared from rat tails as described [2].…”

Section: Methodsmentioning

confidence: 99%

A New ex vivo Model to Study Venous Angiogenesis and Arterio-Venous Anastomosis Formation

et al. 2005

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“…For confocal and fluorescent microscopy, aortic cultures were fixed in 10% buffered formalin for 20 min and processed as whole mounts for fluorescent staining as described [14]. The cultures were washed with water, blocked for 1 h with 5% normal goat serum in phosphate-buffered saline (PBS) or PBS with 0.1% Tween 20 (Sigma), and stained for 1 h with monoclonal antibodies against β 1 integrin (hamster anti-mouse; BD Pharmingen), β 3 integrin (mouse anti-rat; BD Pharmingen), α-SMA (mouse anti-human; Dako, Carpinteria, Calif., USA), vimentin (Dako) or a polyclonal rabbit antibody against von Willebrand Factor (vWF; Sigma).…”

Section: Methodsmentioning

confidence: 99%

Regulation of Postangiogenic Neovessel Survival by β<sub>1</sub> and β<sub>3 </sub>Integrins in Collagen and Fibrin Matrices

et al. 2006

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We used the aortic ring model of angiogenesis to investigate the role of β₁ and β₃ integrins in postangiogenic vascular survival in collagen and fibrin matrices. Confocal microscopy studies showed that both β₁ and β₃ integrins were expressed in endothelial cells and pericytes of sprouting neovessels. Antibody blocking experiments demonstrated that β₁ integrins but not β₃ integrins were required for angiogenic sprouting in collagen. Conversely, in fibrin, blockade of both integrins was needed to inhibit angiogenesis whereas treatment with either antibody alone was ineffective. Antibody-mediated blockade of β₁ but not β₃ integrins accelerated vascular regression in collagen. In contrast, both anti-β₁ and -β₃ integrin antibodies were required to promote neovessel breakdown in fibrin. These results demonstrate that angiogenic sprouting and postangiogenic neovessel survival in collagen are critically dependent on β₁ integrins. They also indicate that these processes involve a redundant repertoire of β₁ and β₃ integrins when angiogenesis occurs in fibrin. Thus, pharmacologic targeting of integrin receptors aimed at blocking neovessel formation and survival must be tailored to the specific extracellular matrix environment in which angiogenesis takes place.

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“…The thin gel rat aortic ring assay was conducted as specified by Zhu and Nicosia [31]. All experiments performed with animals conformed to University of Washington Institutional Animal Care and use Committee guidelines.…”

Section: Rat Aortic Ring Modelmentioning

confidence: 99%

Osteoprotegerin and RANKL differentially regulate angiogenesis and endothelial cell function

2008

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Osteoprotegerin (OPG) a soluble tumor necrosis factor receptor family molecule protects endothelial cells from apoptosis in vitro and promotes neovascularization in vivo. In this study, we assessed the role of OPG and its ligands, receptor activator of nuclear factor-kappaB ligand (RANKL) and tumor necrosis factor-related apoptosis inducing ligand (TRAIL), in microvessel formation using the rat aortic ring model of angiogenesis. OPG was found to promote a twofold increase in angiogenic sprouting in the aortic ring model, and this effect was inhibited by pre-incubation with a fivefold molar excess of either RANKL or TRAIL. While TRAIL had no effect upon angiogenesis on its own, RANKL was found to potently inhibit basal and vascular endothelial growth factor-induced angiogenesis. OPG increased the rate of endothelial cell proliferation in sprouting microvessels; in contrast, RANKL inhibited proliferation. RANKL was found to induce endothelial apoptosis at days 6, 7, and 10 in the aortic ring model and after incubation with human umbilical vein endothelial cells (HUVECs). Signaling studies showed that OPG induced ERK1/2 and Akt phosphorylation in HUVECs while RANKL had no effect. Our results indicate that OPG is a positive regulator of microvessel formation, while RANKL is an angiogenic inhibitor due to effects on regulation of endothelial cell proliferation, apoptosis, and signaling.

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Cited by 65 publications

References 21 publications

A New ex vivo Model to Study Venous Angiogenesis and Arterio-Venous Anastomosis Formation

A New ex vivo Model to Study Venous Angiogenesis and Arterio-Venous Anastomosis Formation

Regulation of Postangiogenic Neovessel Survival by β<sub>1</sub> and β<sub>3 </sub>Integrins in Collagen and Fibrin Matrices

Osteoprotegerin and RANKL differentially regulate angiogenesis and endothelial cell function

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