May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Angiopoietin 1 (Ang1) Decreases Ocular Neovascularization (NV) and VEGF-Induced Breakdown of the Blood-Retinal Barrier (BRB)
H. Nambu; R. Nambu; Y. Oshima; E. Duh; S.F. Hackett; D.J. Zack; P.A. Campochiaro
Author Affiliations & Notes
  • H. Nambu
    Ophthalmology, Wilmer Eye Inst JHU, Baltimore, MD, United States
  • R. Nambu
    Ophthalmology, Wilmer Eye Inst JHU, Baltimore, MD, United States
  • Y. Oshima
    Ophthalmology, Wilmer Eye Inst JHU, Baltimore, MD, United States
  • E. Duh
    Ophthalmology, Wilmer Eye Inst JHU, Baltimore, MD, United States
  • S.F. Hackett
    Ophthalmology, Wilmer Eye Inst JHU, Baltimore, MD, United States
  • D.J. Zack
    Ophthalmology, Wilmer Eye Inst JHU, Baltimore, MD, United States
  • P.A. Campochiaro
    Ophthalmology, Wilmer Eye Inst JHU, Baltimore, MD, United States
  • Footnotes
    Commercial Relationships  H. Nambu, None; R. Nambu, None; Y. Oshima, None; E. Duh, None; S.F. Hackett, None; D.J. Zack, None; P.A. Campochiaro, None.
  • Footnotes
    Support  NIH Grant EY05951, EY12609
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 2901. doi:
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      H. Nambu, R. Nambu, Y. Oshima, E. Duh, S.F. Hackett, D.J. Zack, P.A. Campochiaro; Angiopoietin 1 (Ang1) Decreases Ocular Neovascularization (NV) and VEGF-Induced Breakdown of the Blood-Retinal Barrier (BRB) . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2901.

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Abstract

Abstract: : Purpose: To investigate the role of ang1 in the retina. Methods: Tetracycline response element (TRE)/murine ang1 (TRE/ang1)transgenic mice were generated and crossed with reverse tetracycline transactivator(rtTA)/rhodopsin promoter (rtTA/rho) or rtTA/CMV promoter (rtTA/CMV) mice to generate double transgenics. Expression of ang1 was evaluated by RT-PCR and immunohistochemistry. Mice with doxycycline (dox)-inducible ubiquitous expression of ang1 (rtTA/CMV-TRE/ang1) or dox-inducible expression of ang1 in the retina (rtTA/rho-TRE/ang1) were used to investigate the effect of increased expression of ang1 on ischemic retinopathy, choroidal NV (CNV), and VEGF-induced breakdown of the BRB. Results: Oxygen-induced ischemic retinopathy was generated using litters of newborn rtTA/CMV-TRE/ang1 mice treated with dox or single hemizygous controls. Dox-treated double transgenics had increased ang1 mRNA and protein in the retina and significantly less retinal NV than controls. Adult rtTA/CMV-TRE/ang1 mice with laser-induced rupture of Bruch's membrane that were treated with 2 mg/ml of dox in their drinking water had significantly smaller areas of CNV at rupture sites than controls. Adult rtTA/rho-TRE/ang1 mice were given 2 mg/ml of dox in drinking water for 2 weeks and then received an intravitreous injection of 1 ml of 10-6 M VEGF as did controls. Six hours after injection, the integrity of the BRB was quantitatively assessed using [3H]mannitol as tracer. Mice with dox-induced expression of ang1 had significantly less breakdown of the BRB. Conclusions: Increased expression of ang1 in the retina suppresses the development of ischemia-induced retinal NV, CNV at Bruch's membrane rupture sites, and VEGF-induced breakdown of the BRB. These data suggest that increasing expression of ang1 in the retina provides a potential strategy for treatment of macular edema and retinal neovascularization in patients with ischemic retinopathies, or prevention of CNV in high-risk AMD patients.

Keywords: neovascularization • transgenics/knock-outs • animal model 
© 2003, The Association for Research in Vision and Ophthalmology, Inc., all rights reserved. Permission to republish any abstract or part of an abstract in any form must be obtained in writing from the ARVO Office prior to publication.
Copyright © 2025 Association for Research in Vision and Ophthalmology.
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