[Retinal pigment epithelial cells contribute to maturation and fenestration of the vascular endothelial cells in vascular endothelial growth factor-transgenic mice].

Purpose: To demonstrate the role of the retinal pigment epithelial cells (RPE) in subretinal neovascularization during maturation and fenestration of endothelial cells in vascular endothelial growth factor (VEGF) transgenic mice.

Methods: VEGF transgenic mice were given an intraperitoneal injection of 50 mg/kg of sodium iodate (treated) or physiological saline (controls) on postnatal day 10. Fluorescein angiography (FAG) was carried out and the mice were sacrificed on postnatal day 31.

EST analysis of mouse retina and RPE/choroid cDNA libraries.

Purpose: cDNA libraries from the mouse retina have recently been reported, but no well characterized library from the retinal pigment epithelium (RPE) or choroid of the mouse has yet appeared in the literature. To complement these libraries and to provide the first mouse RPE/choroid library, we used freshly dissected tissue from adult C57BL/6J mice to construct new retina and RPE/choroid libraries.

Methods: Eyes from 100 six to eight week old C57BL/6J mice were dissected in groups of 10.

Ultrastructural aging of the RPE-Bruch's membrane-choriocapillaris complex in the D-galactose-treated mouse.

Purpose: Low-dose D-galactose treatment in mice induces accelerated aging due to advanced glycation endproduct (AGEs) formation. The purpose of this study was to identify ultrastructural aging in the retinal pigment epithelium (RPE)-Bruch's membrane-choriocapillaris.

Methods: Five-month-old C57Bl6 mice were injected daily with D-galactose or control buffer for 8 weeks.

RPE cells modulate subretinal neovascularization, but do not cause regression in mice with sustained expression of VEGF.

Purpose: Previous studies using models of choroidal neovascularization (CNV) in which the angiogenic stimulus is not sustained, have concluded that the retinal pigmented epithelium (RPE) causes regression of neovascularization (NV). However, the withdrawal of angiogenic stimuli may actually be the major modulator of NV, and RPE cells may simply be responding to withdrawal of the angiogenic stimuli or something released by NV because of the withdrawal. In this study, the long-term course of NV and the behavior of the RPE in rhodopsin/VEGF transgenic mice, in which there is a sustained angiogenic stimulus, was investigated.

Age-related changes in the transcriptional profile of mouse RPE/choroid.

To evaluate the age-related changes in gene expression occurring in the complex of retinal pigmented epithelium, Bruch's membrane, and choroid (RPE/choroid), we examined the gene expression profiles of young adult (2 mo) and old (24 mo) male C57BL/6 mice. cDNA probe sets from individual animals were synthesized using total RNA isolated from the RPE/choroid of each animal. Probes were amplified using the Clontech SMART system, radioactively labeled, and hybridized to two different Clontech Atlas mouse cDNA arrays.

Acute hyperoxia-induced transcriptional response in the mouse RPE/choroid.

Oxidative stress has been studied in the retinal pigmented epithelium (RPE) in vitro but not in vivo. Our purpose, therefore, was to develop an in vivo model of acute oxidative stress in the C57BL/6J mouse. Mice were exposed to > or = 98% oxygen for 0, 2, or 6 h, and amplified total RNA from the RPE/choroid was applied to microarrays examining about 2200 unique genes.