Blood vessel anastomosis is spatially regulated by Flt1 during angiogenesis

Nesmith, Jessica E.; Chappell, John C.; G., Cluceru, Julia; Bautch, Victoria L.

doi:10.1242/dev.145672

Cited by 48 publications

(52 citation statements)

References 38 publications

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“…Anastomosis has been included in several 2D and 3D models (Zheng et al, 2013 ; Norton and Popel, 2016 ). ECs with a reduced concentration of membrane-localized VEGFR1 are more likely to form stable connections with incoming sprouts (Nesmith et al, 2017 ). A multicellular model that integrates VEGFR1 regulation, and how it affects anastomosis, may help explain micro–vascular architecture.…”

Section: Discussionmentioning

confidence: 99%

A Network Model to Explore the Effect of the Micro-environment on Endothelial Cell Behavior during Angiogenesis

et al. 2017

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Angiogenesis is an important adaptation mechanism of the blood vessels to the changing requirements of the body during development, aging, and wound healing. Angiogenesis allows existing blood vessels to form new connections or to reabsorb existing ones. Blood vessels are composed of a layer of endothelial cells (ECs) covered by one or more layers of mural cells (smooth muscle cells or pericytes). We constructed a computational Boolean model of the molecular regulatory network involved in the control of angiogenesis. Our model includes the ANG/TIE, HIF, AMPK/mTOR, VEGF, IGF, FGF, PLCγ/Calcium, PI3K/AKT, NO, NOTCH, and WNT signaling pathways, as well as the mechanosensory components of the cytoskeleton. The dynamical behavior of our model recovers the patterns of molecular activation observed in Phalanx, Tip, and Stalk ECs. Furthermore, our model is able to describe the modulation of EC behavior due to extracellular micro-environments, as well as the effect due to loss- and gain-of-function mutations. These properties make our model a suitable platform for the understanding of the molecular mechanisms underlying some pathologies. For example, it is possible to follow the changes in the activation patterns caused by mutations that promote Tip EC behavior and inhibit Phalanx EC behavior, that lead to the conditions associated with retinal vascular disorders and tumor vascularization. Moreover, the model describes how mutations that promote Phalanx EC behavior are associated with the development of arteriovenous and venous malformations. These results suggest that the network model that we propose has the potential to be used in the study of how the modulation of the EC extracellular micro-environment may improve the outcome of vascular disease treatments.

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Section: Discussionmentioning

confidence: 99%

A Network Model to Explore the Effect of the Micro-environment on Endothelial Cell Behavior during Angiogenesis

et al. 2017

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“…Blood vessel formation is primarily achieved by angiogenesis-EC sprouting from pre-existing vessels. Vessel networks expand when sprouts form new connections, and vessel anastomosis is spatially regulated by VEGFR1 (Flt1), a VEGF-A receptor that acts as a decoy receptor [73]. VEGFR1 modulates the activity of VEGFR2, which is the chief pathway in vasculogenesis and angiogenesis.…”

Section: Vwfmentioning

confidence: 99%

Markers and Biomarkers of Endothelium: When Something Is Rotten in the State

Гончаров

Nadeev

Jenkins

et al. 2017

Oxidative Medicine and Cellular Longevity

159

115

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Endothelium is a community of endothelial cells (ECs), which line the blood and lymphatic vessels, thus forming an interface between the tissues and the blood or lympha. This strategic position of endothelium infers its indispensable functional role in controlling vasoregulation, haemostasis, and inflammation. The state of endothelium is simultaneously the cause and effect of many diseases, and this is coupled with modifications of endothelial phenotype represented by markers and with biochemical profile of blood represented by biomarkers. In this paper, we briefly review data on the functional role of endothelium, give definitions of endothelial markers and biomarkers, touch on the methodological approaches for revealing biomarkers, present an implicit role of endothelium in some toxicological mechanistic studies, and survey the role of reactive oxygen species (ROS) in modulation of endothelial status.

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“…The formation of blood vessels is mainly due to angiogenesis, that is, the sprouting of ECs from existing vessels. The vascular network expands when sprouts form new connections, and vascular anastomoses are spatially regulated by VEGFR1 (Flt1), which acts as a trap receptor [72]. VEGFR1 modulates the activity of VEGFR2, the main regulator of vasculogenesis and angiogenesis.…”

Section: Vwfmentioning

confidence: 99%

Markers of Endothelial Cells in Normal and Pathological Conditions

Гончаров

Попова

Avdonin

et al. 2020

Biochem. Moscow Suppl. Ser. A

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Endothelial cells (ECs) line the blood vessels and lymphatic vessels, as well as heart chambers, forming the border between the tissues, on the one hand, and blood or lymph, on the other. Such a strategic position of the endothelium determines its most important functional role in the regulation of vascular tone, hemostasis, and inflammatory processes. The damaged endothelium can be both a cause and a consequence of many diseases. The state of the endothelium is indicated by the phenotype of these cells, represented mainly by (trans)membrane markers (surface antigens). This review defines endothelial markers, provides a list of them, and considers the mechanisms of their expression and the role of the endothelium in certain pathological conditions.

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Blood vessel anastomosis is spatially regulated by Flt1 during angiogenesis

Cited by 48 publications

References 38 publications

A Network Model to Explore the Effect of the Micro-environment on Endothelial Cell Behavior during Angiogenesis

A Network Model to Explore the Effect of the Micro-environment on Endothelial Cell Behavior during Angiogenesis

Markers and Biomarkers of Endothelium: When Something Is Rotten in the State

Markers of Endothelial Cells in Normal and Pathological Conditions

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