May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Angiopoietin 1 Prevents Retinal Detachment in an Aggressive Model of Proliferative Retinopathy, but Has No Effect on Established Neovascularization
Author Affiliations & Notes
  • N. Umeda
    Dept of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University, Baltimore, MD
  • H. Nambu
    Dept of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University, Baltimore, MD
  • S. Kachi
    Dept of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University, Baltimore, MD
  • Y. Oshima
    Dept of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University, Baltimore, MD
  • H. Akiyama
    Dept of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University, Baltimore, MD
  • R. Nambu
    Dept of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University, Baltimore, MD
  • P.A. Campochiaro
    Dept of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University, Baltimore, MD
  • Footnotes
    Commercial Relationships  N. Umeda, None; H. Nambu, None; S. Kachi, None; Y. Oshima, None; H. Akiyama, None; R. Nambu, None; P.A. Campochiaro, None.
  • Footnotes
    Support  EY05951, EY12609, and core grant P30EY1765 from the NEI
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 4193. doi:
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      N. Umeda, H. Nambu, S. Kachi, Y. Oshima, H. Akiyama, R. Nambu, P.A. Campochiaro; Angiopoietin 1 Prevents Retinal Detachment in an Aggressive Model of Proliferative Retinopathy, but Has No Effect on Established Neovascularization . Invest. Ophthalmol. Vis. Sci. 2005;46(13):4193.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: Vascular endothelial growth factor (VEGF) plays a central role in vasoproliferative diseases in the retina, however other gene products modulate its effect. The angiopoietins are particularly important in this regard. Angiopoietin 2 (Ang2) collaborates with VEGF to stimulate neovascularization (NV) in some situations, but in other situations causes regression of NV. Ang2 also causes a transient increase in vascular density during retinal vascular development. In this study we sought to determine if Ang1 has similar activities. Methods: Double transgenic mice with inducible expression of Ang1 in the retina were used to explore the effects of Ang1 in models of ocular NV. Results: Increased expression of Ang1 in the retina during retinal vascular development did not cause a detectable alteration in vascular density. Also, unlike Ang2, increased expression of Ang1 had no effect on established retinal or choroidal NV. However, when Ang1 expression was initiated simultaneously with that of VEGF, it strongly suppressed VEGF–induced NV and prevented retinal detachment. Conclusions: These data indicate that the timing of Ang1 expression is a critical determinate of its effects on VEGF–induced NV in the retina; it effectively blocks the initiation and progression of NV, but cannot reverse established NV or reduce leakage from NV. These data suggest that increased expression of Ang1 may be a good strategy for prophylaxis of retinal NV, but is unlikely to be effective as monotherapy of established NV.

Keywords: retinal neovascularization • choroid: neovascularization • transgenics/knock-outs 
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