April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
HIF-1 Regulated Gene Therapy Reduces Choroidal Neovascularization in a Mouse-Model
Author Affiliations & Notes
  • G. W. Smith
    Center for Complex Systems and Brain Sci,
    Florida Atlantic University, Boca Raton, Florida
  • E. Hernandez
    Bascom Palmer Eye Institute, University of Miami, Miller School of Medicine, Miami, Florida
  • H. Prentice
    Charles E. Schmidt College of Biomedical Science,
    Florida Atlantic University, Boca Raton, Florida
  • C. Dorey
    Virginia Tech Carilion School of Medicine, Roanoke, Virginia
  • M. Biswal
    Center for Complex Systems and Brain Sci,
    Florida Atlantic University, Boca Raton, Florida
  • T. House
    Center for Complex Systems and Brain Sci,
    Florida Atlantic University, Boca Raton, Florida
  • J. Blanks
    Center for Complex Systems and Brain Sci,
    Florida Atlantic University, Boca Raton, Florida
  • Footnotes
    Commercial Relationships  G.W. Smith, None; E. Hernandez, None; H. Prentice, None; C. Dorey, None; M. Biswal, None; T. House, None; J. Blanks, None.
  • Footnotes
    Support  NIH grant EYO16119; NIH grant P30 EY014801-01A1; AHA pre-doctoral fellowship 0815022E (M. Biswal)
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 4495. doi:
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      G. W. Smith, E. Hernandez, H. Prentice, C. Dorey, M. Biswal, T. House, J. Blanks; HIF-1 Regulated Gene Therapy Reduces Choroidal Neovascularization in a Mouse-Model. Invest. Ophthalmol. Vis. Sci. 2010;51(13):4495.

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

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Abstract

Purpose: : Choroidal neovascularization (CNV) in age-related macular degeneration (AMD) is strongly associated with hypoxia and chronic inflammation. These events typically precede CNV, and are thought to play an underlying role in the induction of the neovascular process. HIF-1 is a transcription factor that is vital in regulating cellular responses to hypoxic and inflammatory conditions. In order to inhibit CNV, we have engineered a viral vector that uses HIF-1 regulation to exploit the pathological conditions in the AMD retina in order to stimulate local production of an angiostatic protein. The purpose of this study was to investigate the effects of a HIF-1 regulated, RPE-specific gene therapy platform in a mouse-model of CNV.

Methods: : 1uL of our HIF-1 regulated, RPE-specific self-complimentary vector (scAAV2-HRSE-HRE-RPE65-hrEndostatin), scAAV2-CMV-Endostatin, or vehicle control was injected subretinally in 6-9 month old C57BL/6 mice. approximately one week post-injection a 532nm diode laser was used to induce CNV (100uM spot size, 150mW power, & 0.1s duration). Three spots per eye were lasered; two weeks post-laser injury the mice were perfused with a FITC-conjugated tomato lectin. The eyes were then enucleated and RPE/Choroid/Sclera flatmounts were made and coverslipped. Confocal microscope images of fluorescent vessels and CNV areas within the lesions were quantified using Image J.

Results: : CNV area was 80% smaller (P<0.0001) in eyes treated with the HIF-1 regulated, RPE-specific endostatin vector than in the vehicle injected eyes. CNV was also significantly reduced in eyes treated with the CMV-endostatin vector.

Conclusions: : Although both scAAV2-CMV-Endostatin and scAAV2-HRES-HRE-RPE-Endostatin significantly reduce CNV, it is unknown whether broad and constitutive endostatin expression will have damaging effects within the retina. Our results indicate that a local, regulated expression can effectively inhibit CNV, and offers the further possibility of a prophylactic treatment for neovascular AMD.

Keywords: gene transfer/gene therapy • retina • neovascularization 
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