April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
LRP5 Is a Potential Target for Anti-intraretinal Angiogenesis
Author Affiliations & Notes
  • Chun-hong Xia
    School of Optometry, University of California, Berkeley, Berkeley, California
  • Eric Lu
    School of Optometry, University of California, Berkeley, Berkeley, California
  • Xiaohua Gong
    School of Optometry, University of California, Berkeley, Berkeley, California
  • Footnotes
    Commercial Relationships  Chun-hong Xia, None; Eric Lu, None; Xiaohua Gong, None
  • Footnotes
    Support  NIH grant EY013849 and a grant from the East Bay Community Foundation.
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 3124. doi:
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    • Get Citation

      Chun-hong Xia, Eric Lu, Xiaohua Gong; LRP5 Is a Potential Target for Anti-intraretinal Angiogenesis. Invest. Ophthalmol. Vis. Sci. 2011;52(14):3124.

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

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Abstract

Purpose: : To understand the underlying mechanisms for the opposite retinal vasculature phenotypes in the loss-of-function mutant mice of low-density lipoprotein receptor-related protein 5 (LRP5) and very low-density lipoprotein receptor (VLDLR). To characterize the retinal vasculature defect in mice lacking both LRP5 and VLDLR.

Methods: : Fundus examination, fluorescein angiography, immunostaining, and 3-dimensional retinal vasculature reconstruction were performed to evaluate the molecular and cellular alterations of retinal vasculature in mutant animals.

Results: : A loss of LRP5 in mice leads to an undergrowth of the intraretinal vasculature, the formation of endothelial cell (EC) clusters, and a failure of ECs to migrate into deeper retinal layers. In contrast, VLDLR knockout mice show an overgrowth of the intraretinal vasculature and subretinal neovascularization. Thus, LRP5 mediates a pro-angiogenic signal and VLDLR mediates an anti-angiogenic signal. Using the LRP5/VLDLR double knockout (DKO) mice, we have genetically tested whether a loss-of-function of LRP5 is able to prevent the neovascularization caused by VLDLR gene mutations. Our data reveal that retinal vessels fail to grow into the photoreceptor layer in the DKO mice.

Conclusions: : LRP5 and VLDLR, members of the LDL receptor family, play opposite roles during retinal angiogensis. LRP5 is a prerequisite for the overgrowth of retinal vasculature in the VLDLR knockout mice. Thus, inhibition of LRP5 function is a potential novel approach to prevent intraretinal angiogenesis.

Keywords: retina • mutations • retinal neovascularization 
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