May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
Increased Laser–Induced Choroidal Neovascularization in Mice Lacking Collagen XVIII/Endostatin
A.G. Marneros; H. Zambarakji; H. She; H. Hashizume; E.J. Connolly; E.S. Gragoudas; B.R. Olsen; J.W. Miller
Author Affiliations & Notes
  • A.G. Marneros
    Oral and Developmental Biology, Harvard Medical School/Harvard Dental School, Boston, MA
  • H. Zambarakji
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, MA
  • H. She
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, MA
  • H. Hashizume
    Research Pharmacology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
  • E.J. Connolly
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, MA
  • E.S. Gragoudas
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, MA
  • B.R. Olsen
    Oral and Developmental Biology, Harvard Medical School/Harvard Dental School, Boston, MA
  • J.W. Miller
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, MA
  • Footnotes
    Commercial Relationships  A.G. Marneros, None; H. Zambarakji, None; H. She, None; H. Hashizume, None; E.J. Connolly, None; E.S. Gragoudas, None; B.R. Olsen, None; J.W. Miller, None.
  • Footnotes
    Support  NIH Grant AR36820; Ruth and Milton Steinbach Fund; Core Grant for Vision Research P30EY14104; T.F.C Frost Trust and the Cripplegate and Dowsett Fellowship
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 1532. doi:
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      A.G. Marneros, H. Zambarakji, H. She, H. Hashizume, E.J. Connolly, E.S. Gragoudas, B.R. Olsen, J.W. Miller; Increased Laser–Induced Choroidal Neovascularization in Mice Lacking Collagen XVIII/Endostatin . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1532.

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Abstract

Purpose: : To determine whether the lack of physiological levels of collagen XVIII/endostatin affects the development of laser–induced choroidal neovascularization (CNV).

Methods: : Age–matched groups of adult Col18a1–/– mice and littermate control mice on the C57BL/6J genetic background were used for all experiments. Ultrastructural analysis of the choroidal vasculature was performed to exclude an underlying vascular abnormality between mutant and control mice. Laser photocoagulation was used to induce CNV in each quadrant of the fundus. Two weeks after laser injury, CNV lesions were assessed using masked grading of fluorescein angiographic leakage and by CNV size using FITC–dextran perfused choroidal flat–mounts. The CNV lesions were also evaluated histologically. In addition, retinal VEGF expression was assessed.

Results: : Choroidal vessels contain collagen XVIII and endostatin in their subendothelial basement membrane. Lack of collagen XVIII does not alter the ultrastructure of the choroidal vasculature in Col18a1–/– mice. Two weeks after laser induction of CNV, mutant mice showed significantly increased CNV lesion size when compared to control littermates. In addition, CNV lesions fused to form large subretinal neovascular complexes in Col18a1–/– mice. The observed differences in laser–induced CNV were also noted in aged mice. Increased CNV lesion size in Col18a1–/– mice was associated with higher retinal VEGF expression in these mice when compared to control mice.

Conclusions: : These data indicate a role for collagen XVIII/endostatin in the development of experimental CNV, and suggest that physiological levels of collagen XVIII/endostatin can regulate induced angiogenesis in vivo. The collagen XVIII/endostatin null mice are the first mutant mice to show increased experimental CNV due to the lack of a single basement membrane component.

Keywords: choroid: neovascularization • Bruch's membrane • age-related macular degeneration 
© 2006, 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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