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W. Hu, J. Liang, B. Chang, H. Gao, X. Qiao; Loss of VLDL Receptor in the RPE Cell Is Involved in the Initial Stage of Subretinal Neovascularization in vldlr-/- Mice. Invest. Ophthalmol. Vis. Sci. 2007;48(13):1738.
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© ARVO (1962-2015); The Authors (2016-present)
To establish the normal pattern of very low density lipoprotein receptor (VLDLR) expression in the retina, and to investigate whether loss of VLDLR in the retina may contribute to the development of subretinal neovascularization in the VLDLR knockout (vldlr-/-) mice.
RT-PCR was performed to detect the mRNA expression of VLDLR in the retina and isolated RPE cells of adult wildtype mice. Immunohistochemistry was used to localize the expression pattern of VLDLR protein in the mouse retina. Ocular tissues from 3 week old vldlr-/- mice were serially sectioned for histological analysis. High molecular weight FITC-dextran angiography in RPE-choroid-sclera flat mounts with anti-elastin immunostaining was used to identify RPE cell destruction and Bruch’s membrane exposure.
Both mRNA and protein of VLDLR were detected in the retina with most intense staining in the RPE of the wildtype mice. In the vldlr-/- mice, VLDLR expression was not detected in the retina. Thhere were significant growth of neovascular proliferations in the subretinal space at 3 weeks of age. However, not all of the subretinal lesions corresponded with morphological disturbance in the outer plexiform layer. Choroidal flat mount FITC-dextran angiography revealed positive elastin staining of the Bruch’s membrane in the lesion sites of subretinal neovascularization, demonstrating the disruption of RPE layer.
The VLDLR is expressed in the retina and RPE cells of the wildtype mice. Loss of VLDLR in the RPE may be involved in the destruction of the RPE cells with subsequent development of subretinal neovascularization in vldlr-/- mice.
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