The bst locus on mouse chromosome 16 is associated with age-related subretinal neovascularization.

Document Type

Article

Publication Date

2000

Keywords

Animal, Chromosome-Mapping, Disease-Models-Animal, Eye, Fluorescein-Angiography, Mice, Mice-Inbred-C57BL, Retinal-Neovascularization, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-P-H-S

First Page

2191

Last Page

2195

JAX Source

Proc Natl Acad Sci USA 2000 Feb; 97(5):2191-5.

Grant

RO1EY07758/EY/NEI, RR01183/RR/NCRR, CA34196/CA/NCI

Abstract

Ocular neovascularization is the leading cause of blindness in developed countries and often causes rapid loss of vision in age-related macular degeneration. Acute visual loss is most often due to hemorrhage from new vessels that have extended from the choroid into the subretinal space. Growth of abnormal vessels beneath the retina in this condition is known as subretinal neovascularization (SRN). Age-related animal models of macular degeneration and SRN have not been described. Current animal models of SRN depend on chemical or physical stimuli to initiate growth of subretinal vessels. The genes responsible for age-related human macular degeneration with SRN have not been firmly identified. We report an angiogenic phenotype in Bst/+ mice that is age-related, clinically evident, and resembles human SRN. This represents a spontaneous, genetically determined model of SRN. Bst/+ mice offer the possibility of exploring the molecular mechanisms of SRN without the need for exogenous agents.

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