NDLI: The role of Vldlr in intraretinal angiogenesis in mice.

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The role of Vldlr in intraretinal angiogenesis in mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Liu, Haiquan Du, Xin Beutler, Bruce Gong, Xiaohua Xia, Chun-Hong Lu, Eric
Description	Country affiliation: United States Author Affiliation: Xia CH ( School of Optometry and Vision Science Program, University of California, Berkeley, USA. chxia@berkeley.edu)
Abstract	PURPOSE. To identify and characterize the r26 mouse line, which displays depigmented patches in the retina, and to determine the causative gene mutation and study the underlying mechanism. METHODS. Fundus examination, fluorescein angiography, histology, and immunostaining were used to determine the retinal phenotypes. Genome-wide linkage analysis, DNA sequencing, and an allelic test were used to identify the causative gene mutation. Wild-type and mutant gene products were examined by Western blot and transient transfection. RESULTS. Homozygous r26/r26 mice displayed depigmented patches in the fundus that overlapped the hyperfluorescent spots in the angiogram. Histology showed overgrown retinal vessels in the subretinal space. Immunostaining verified the presence of endothelial cells in the photoreceptor layer. Chromosome mapping and DNA sequencing revealed a point mutation, c.2239C>T, in the very-low-density lipoprotein receptor (Vldlr) gene. An allelic test in Vldlr knockout (-/-) mice confirmed that r26/(-) mice display a phenotype similar to that of r26/r26 mice. The Vldlr protein was predominantly localized at the plasma membrane of transfected cells, whereas the truncated Vldlr was diffusely expressed in the cell cytosol. The r26 truncated Vldlr was undetectable in mutant retinas by Western blot. CONCLUSIONS. The r26 is a recessive mutant caused by a missense mutation in the Vldlr gene. This results in a truncated Vldlr protein that lacks the C-terminal 127 amino acid residues including the single transmembrane domain and fails to localize at the plasma membrane. Thus, the r26 is a loss-of-function Vldlr mutation. Vldlr on the cell surface probably mediates an antiangiogenic signal to prevent retinal endothelial cells from migrating into the photoreceptor cell layer.
ISSN	01460404
e-ISSN	15525783
DOI	10.1167/iovs.10-7082
Journal	Investigative Opthalmology & Visual Science
Issue Number	9
Volume Number	52
Language	English
Publisher	Association for Research in Vision and Ophthalmology
Publisher Date	2011-08-22
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Mutation, Missense Point Mutation Receptors, Ldl Physiology Retinal Neovascularization Genetics Retinitis Pigmentosa Animals Blotting, Western Ethylnitrosourea Toxicity Fluorescein Angiography Genetic Complementation Test Genome-wide Association Study Mice Mice, Inbred C3h Mice, Inbred C57bl Mice, Knockout Mice, Mutant Strains Phenotype Chemically Induced Pathology Retinal Vessels Sequence Analysis, Dna Transfection Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Ophthalmology
Content Type	Text
Resource Type	Article
Subject	Ophthalmology Sensory Systems Cellular and Molecular Neuroscience

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