This Article  • Full text  • PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Citing articles on ISI (1)  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Topic Collections  • Nutritional and Metabolic Disorders  • Lipids and Lipid Disorders  • Macular Degeneration  • Retinal/ Chorioretinal Disorders  • Alert me on articles by topic  Social Bookmarking   What's this?

An Animal Model of Retinal Angiomatous Proliferation

Chao Li, MD; Zhong Huang, MD, PhD; Ronald Kingsley, MD; Xiaohong Zhou, MD, PhD; Feng Li, MD; David W. Parke II, MD; Wei Cao, MD, PhD

Arch Ophthalmol. 2007;125(6):795-803.

Objective  To identify and characterize biochemical alterations in the retinas of very low-density lipoprotein receptor (VLDLr) knockout mice in an animal model of retinal angiomatous proliferation.

Methods  Immunohistochemical analysis, Western blot analysis, reverse transcriptase–polymerase chain reaction, and electrophoretic mobility shift assay were used to identify and characterize the altered gene and protein expression as well as signal cascades involved in the pathogenesis of neovascularization in the retinas of VLDLr mice.

Results  Expression of the angiogenic factors vascular endothelial growth factor and basic fibroblast growth factor was significantly greater in the lesion area, and Müller cells around the lesion area were activated, as indicated by increased expression of glial fibrillary acidic protein. Expression of the proinflammatory cytokine IL-18 (interleukin 18) and the inflammation mediator intercellular adhesion molecule-1 was increased before significant intraretinal neovascularization. Furthermore, phosphorylation of Akt and mitogen-activated protein kinase and translocalization of nuclear factor kappa B were greater in VLDLr knockout mouse retinas.

Conclusion  An inflammatory process is involved in the development of neovascularization in the VLDLr knockout mouse retina.

Clinical Relevance  Understanding the molecular mechanisms underlying these biochemical alterations in the retinas of VLDLr knockout mice will provide a foundation for developing novel therapeutic approaches to retinal angiomatous proliferation.

Author Affiliations: Department of Ophthalmology, University of Oklahoma Health Science Center and Dean A. McGee Eye Institute, Oklahoma City.

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Loss of VLDL Receptor Activates Retinal Vascular Endothelial Cells and Promotes Angiogenesis
Jiang et al.
IOVS 2009;50:844-850.
ABSTRACT | FULL TEXT  

Expression of VLDLR in the Retina and Evolution of Subretinal Neovascularization in the Knockout Mouse Model's Retinal Angiomatous Proliferation
Hu et al.
IOVS 2008;49:407-415.
ABSTRACT | FULL TEXT