May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Retinal and Choroidal Localization of Endostatin in Normal Aged Humans and in Age-Related Macular Degeneration
Author Affiliations & Notes
  • I.A. Bhutto
    Ophthalmology, Johns Hopkins Univ Sch Med, Baltimore, MD, United States
  • S.Y. Kim
    Ophthalmology, Johns Hopkins Univ Sch Med, Baltimore, MD, United States
  • D.S. McLeod
    Ophthalmology, Johns Hopkins Univ Sch Med, Baltimore, MD, United States
  • C.A. Merges
    Ophthalmology, Johns Hopkins Univ Sch Med, Baltimore, MD, United States
  • G.A. Lutty
    Ophthalmology, Johns Hopkins Univ Sch Med, Baltimore, MD, United States
  • Footnotes
    Commercial Relationships  I.A. Bhutto, None; S.Y. Kim, None; D.S. McLeod, None; C.A. Merges, None; G.A. Lutty, None.
  • Footnotes
    Support  Foundation Fighting Blindness Research Grant
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 1729. doi:
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      I.A. Bhutto, S.Y. Kim, D.S. McLeod, C.A. Merges, G.A. Lutty; Retinal and Choroidal Localization of Endostatin in Normal Aged Humans and in Age-Related Macular Degeneration . Invest. Ophthalmol. Vis. Sci. 2003;44(13):1729.

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

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Abstract

Abstract: : Purpose:Endostatin is a proteolytic fragment from the C-terminus of collagen XVIII. It inhibits endothelial cell proliferation in vitro and angiogenesis in vivo. In mouse, collagen XVIII has been demonstrated prominently in all ocular basement membranes except Descemet’s membrane. Also, a collagen XVIII knockout mouse had a delayed regression of the hyaloid vasculature and tunica vasculosa lentis (Fukai et al., EMBO J 21:1535, 2002). Therefore, lack of collagen XVIII/endostatin results in vascular phenotypic changes in mouse. The purpose of this study was to examine the localization of endostatin in human retina and choroid and to determine if the localization or relative levels were changed in age-related macular degeneration (AMD) subjects. Methods:Immunohistochemistry was performed on cryopreserved tissue with a goat anti-mouse endostatin antibody and a streptavidin alkaline phosphatase detection system. Blood vessels were identified in adjacent sections with anti-CD34 antibody. Sections were then bleached to remove melanin. Eyes from four control (mean age 82) and 6 AMD subjects (mean age 87) were studied. Results:In the control subjects, endostatin was in all large retinal blood vessels and in capillaries in some individuals, but the internal limiting membrane (ILM) had the most intense immunostaining. In normal choroid, blood vessels, Bruch’s membrane, and retinal pigment epithelium (RPE) basal lamina had endostatin immunoreactivity. AMD retinas had a similar pattern and intensity of endostatin immunostaining as observed in controls. Endostatin immunoreactivity was sharply reduced in the choriocapillaris, Bruch’s membrane, and RPE basal lamina of AMD choroids and completely negative in some areas of choroid. Conclusions:Endostatin immunostaining was most intense in ILM, Bruch's membrane, and vascular basement membranes. In AMD, endostatin was reduced or absent in Bruch’s membrane, RPE basal lamina, and choriocapillaris. The reduced levels of endostatin in Bruch’s membrane, RPE basal lamina, and choriocapillaris suggests that a decrease in the levels or lack of this endogenous antiangiogenic protein in eyes with AMD may be permissive for choroidal neovascular formation.

Keywords: choroid: neovascularization • growth factors/growth factor receptors • immunohistochemistry 
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