May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
A VEGF121–Gelonin Fusion Protein (VEGF121/rGel) Induces Regression of Subretinal and Choroidal Neovascularization (CNV)
Author Affiliations & Notes
  • H. Akiyama
    Ophthalmology, Wilmer Eye Inst, Baltimore, MD
  • R.L. Silva
    Ophthalmology, Wilmer Eye Inst, Baltimore, MD
  • S. Kachi
    Ophthalmology, Wilmer Eye Inst, Baltimore, MD
  • N. Umeda
    Ophthalmology, Wilmer Eye Inst, Baltimore, MD
  • S. Aslam
    Ophthalmology, Wilmer Eye Inst, Baltimore, MD
  • S.F. Hackett
    Ophthalmology, Wilmer Eye Inst, Baltimore, MD
  • K. Mohamedali
    MD Anderson Cancer Institute, Houston, TX
  • M.G. Rosenblum
    MD Anderson Cancer Institute, Houston, TX
  • P.A. Campochiaro
    Ophthalmology, Wilmer Eye Inst, Baltimore, MD
  • Footnotes
    Commercial Relationships  H. Akiyama, None; R.L. Silva, None; S. Kachi, None; N. Umeda, None; S. Aslam, None; S.F. Hackett, None; K. Mohamedali, None; M.G. Rosenblum, None; P.A. Campochiaro, None.
  • Footnotes
    Support  EY12609
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 455. doi:
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      H. Akiyama, R.L. Silva, S. Kachi, N. Umeda, S. Aslam, S.F. Hackett, K. Mohamedali, M.G. Rosenblum, P.A. Campochiaro; A VEGF121–Gelonin Fusion Protein (VEGF121/rGel) Induces Regression of Subretinal and Choroidal Neovascularization (CNV) . Invest. Ophthalmol. Vis. Sci. 2005;46(13):455.

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

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Abstract

Abstract: : Purpose: Intravascularly injected VEGF121/rGel selectively binds and damages tumor vessels. In this study, the effect of intravascular or intravitreous injection of VEGF121/rGel was tested in two models of ocular neovascularization (NV). Methods: One week after rupture of Bruch’s membrane the baseline amount of CNV was measured in a group of mice and remaining mice received injection of VEGF121/rGel or rGel and after one week the amount of CNV was measured. A similar protocol was used in rho/VEGF mice. VEGF121/rGel was localized in ocular sections by immunohistochemistry. Results: In rho/VEGF mice, intravitreous injections of 0.005 µg VEGF121/rGel starting at postnatal day (P) 21 resulted in a significant reduction in total area of subretinal NV per retina at P25 compared with vehicle–injected mice. In mice with established CNV one week after rupture of Bruch’s membrane, tail vein injections of 45 mg/kg of VEGF121/rGel every two days for 1 week or a single intravitreous injection of 0.005 µg of VEGF121/rGel resulted in significant reductions in CNV area at rupture sites compared with the baseline area before treatment. After intravascular or intravitreous injections, VEGF121/rGel was localized to CNV lesions with no staining of normal retinal or choroidal vessels. Conclusions: These data indicate that after either intravascular or intravitreous injections of VEGF121/rGel, it localizes to new vessels in the eye and causes regression of the neovascularization. Vascular targeting with VEGF121/rGel provides a new approach for inducing regression of ocular NV.

Keywords: drug toxicity/drug effects • choroid: neovascularization • retinal neovascularization 
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