Angiogenesis in the mouse retina: A model system for experimental manipulation

Uemura, Akiyoshi; Kusuhara, Sentaro; Katsuta, Hideto; Nishikawa, Shin‐Ichi

doi:10.1016/j.yexcr.2005.10.030

Cited by 90 publications

(79 citation statements)

References 41 publications

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“…5 online). One vascular bed that is amenable to the analysis of developmental and pathologic angiogenesis is in the neonatal mouse retina [11][12][13]. High-resolution imaging of these blood vessels has demonstrated the existence of two discrete populations of endothelial cells, which possess unique structural and functional characteristics12.…”

mentioning

confidence: 99%

Robo4 stabilizes the vascular network by inhibiting pathologic angiogenesis and endothelial hyperpermeability

Jones

London

Chen

et al. 2008

Nat Med

347

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mentioning

confidence: 99%

Robo4 stabilizes the vascular network by inhibiting pathologic angiogenesis and endothelial hyperpermeability

Jones

London

Chen

et al. 2008

Nat Med

347

451

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“…However, unlike most other parts of the CNS, the retina of rodents becomes vascularized only after birth (for recent comprehensive reviews of retinal vascular development and the retina as a model for angiogenesis research, see refs. 17,18). Vessels emerge from a capillary ring at the optic disk and sprout radially just underneath the inner limiting membrane, the vitreal surface of the retina.…”

Section: The Mouse Retina Modelmentioning

confidence: 99%

VEGF and endothelial guidance in angiogenic sprouting

2008

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The cellular actions of VEGF need to be coordinated to guide vascular patterning during sprouting angiogenesis. Individual endothelial tip cells lead and guide the blood vessel sprout, while neighbouring stalk cells proliferate and form the vascular lumen. Recent studies illustrate how endothelial DLL4/NOTCH signalling, stimulated by VEGF, regulates the sprouting response by limiting tip cell formation in the stalk. The spatial distribution of VEGF, in turn, regulates the shape of the ensuing sprout by directing tip cell migration and determining stalk cell proliferation.

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“…At a macroscopic scale, the trajectories and branch points of major arteries and veins are highly stereotyped, and at a microscopic scale, capillary density within each tissue is governed by characteristic statistical parameters. These attributes are particularly accessible to observation and manipulation in the mammalian retina (1,2). In many mammals, including mice and humans, the retinal vasculature develops by radial migration of endothelial cells (ECs) along the inner (vitreal) face of the retina starting from their point of entry at the optic disk.…”

mentioning

confidence: 99%

Endothelin-2 signaling in the neural retina promotes the endothelial tip cell state and inhibits angiogenesis

Rattner

Williams

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Endothelin signaling is required for neural crest migration and homeostatic regulation of blood pressure. Here, we report that constitutive overexpression of Endothelin-2 (Edn2) in the mouse retina perturbs vascular development by inhibiting endothelial cell migration across the retinal surface and subsequent endothelial cell invasion into the retina. Developing endothelial cells exist in one of two states: tip cells at the growing front and stalk cells in the vascular plexus behind the front. This division of endothelial cell states is one of the central organizing principles of angiogenesis. In the developing retina, Edn2 overexpression leads to overproduction of endothelial tip cells by both morphologic and molecular criteria. Spatially localized overexpression of Edn2 produces a correspondingly localized endothelial response. Edn2 overexpression in the early embryo inhibits vascular development at midgestation, but Edn2 overexpression in developing skin and brain has no discernible effect on vascular structure. Inhibition of retinal angiogenesis by Edn2 requires expression of Endothelin receptor A but not Endothelin receptor B in the neural retina. Taken together, these observations imply that the neural retina responds to Edn2 by synthesizing one or more factors that promote the endothelial tip cell state and inhibit angiogenesis. The response to Edn2 is sufficiently potent that it overrides the activities of other homeostatic regulators of angiogenesis, such as Vegf.

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Angiogenesis in the mouse retina: A model system for experimental manipulation

Cited by 90 publications

References 41 publications

Robo4 stabilizes the vascular network by inhibiting pathologic angiogenesis and endothelial hyperpermeability

Robo4 stabilizes the vascular network by inhibiting pathologic angiogenesis and endothelial hyperpermeability

VEGF and endothelial guidance in angiogenic sprouting

Endothelin-2 signaling in the neural retina promotes the endothelial tip cell state and inhibits angiogenesis

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