May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Therapeutic Potential of Recombinant Membrane-Targeted Form of MAC Regulator CD59 in Laser-Induced CNV
Author Affiliations & Notes
  • P. S. Bora
    Ophthalmology/Jones Eye Institute, Univ of Arkansas for Med Sci, Little Rock, Arkansas
  • S. Kaliappan
    Ophthalmology/Jones Eye Institute, Univ of Arkansas for Med Sci, Little Rock, Arkansas
  • P. Jha
    Ophthalmology/Jones Eye Institute, Univ of Arkansas for Med Sci, Little Rock, Arkansas
  • N. S. Bora
    Ophthalmology/Jones Eye Institute, Univ of Arkansas for Med Sci, Little Rock, Arkansas
  • Footnotes
    Commercial Relationships  P.S. Bora, None; S. Kaliappan, None; P. Jha, None; N.S. Bora, None.
  • Footnotes
    Support  EY014623, EY016205, Research to Prevent Blindness, Inc.NY and the Pat & Willard Walker Eye Research Center, Jones Eye Institute, University of Arkansas for Medical Sciences (Little Rock, AR).
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 293. doi:https://doi.org/
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      P. S. Bora, S. Kaliappan, P. Jha, N. S. Bora; Therapeutic Potential of Recombinant Membrane-Targeted Form of MAC Regulator CD59 in Laser-Induced CNV. Invest. Ophthalmol. Vis. Sci. 2008;49(13):293. doi: https://doi.org/.

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

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Abstract

Purpose: : The present study was undertaken to explore the effect of membrane targeted form of mouse CD59 (rCD59-APT542) on the growth of CNV complex in mice.

Methods: : CNV was induced by laser photocoagulation in C57BL/6 mice using an Argon laser and animals received a single injection of rCD59-APT542 via the intraperitoneal (ip) route on day 3, 5 or 7 post-laser. Control animals received a similar treatment with sterile PBS. Retinal pigment epithelium (RPE)-choroid-scleral flat mounts prepared from the harvested eyes were stained for elastin and the incidence of CNV was determined by confocal microscopy. The size of the CNV complex was graded by morphometric analysis of the images. RPE-choroid-scleral flat mounts were also stained for MAC deposition.

Results: : Administration of membrane-targeted CD59 (rCD59-APT542) inhibited not only the development of CNV complex but also the fully developed CNV in mouse model. The inhibition of CNV in the animals treated with rCD59-APT542 on day 3, 5 and 7 was 77.20%, 82.50% and 75.60% respectively. Day 3 and 5 represent the growth of CNV complex and day 7 represents fully developed CNV. MAC formation was also inhibited in these animals.

Conclusions: : Recombinant membrane targeted CD59 inhibited the growth of CNV complex as well as fully developed CNV in the laser-induced mouse model by inhibiting MAC formation. Our results suggest that complement inhibition at the terminal stage of complement activation using recombinant membrane targeted CD59 is clinically more relevant and would represent a novel and better therapy for human CNV.

Keywords: choroid: neovascularization • inflammation 
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