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R. Wen, Y. Song, L. Zhao, Y. Liu, Y. Li, A.M. Laties; Subretinal Matrigel Induces Translocation of the RPE and Formation of Sub–RPE Deposit . Invest. Ophthalmol. Vis. Sci. 2006;47(13):4151.
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A cardinal pathological feature of age–related macular degeneration (AMD) is the deposition of extracellular material between the retinal pigment epithelium (RPE) and Bruch’s membrane, pathologically described as sub–RPE deposits. Both the presence and local organization of these deposits contribute to the clinical manifestations of AMD, including localized bodies clinically recognized as drusen. The biogenesis of sub–RPE deposits remains elusive.
Matrigel was injected into the subretinal space of adult Long Evans rats to create an amorphous deposit. Eyes were harvested after Matrigel injection and embedded in an Epon–Araldite mixture. Semi–thin tissue sections were cut through the Matrigel injected area and examined by light microscopy.
RPE cells started to leave Bruch’s membrane and migrate toward photoreceptors 5 days after Matrigel injection. They then formed a new layer between Matrigel and photoreceptors, resulting in RPE translocation. The translocated RPE displaces the Matrigel deposit to the location between the RPE and Bruch’s membrane. Since we traditionally use the RPE as a reference to describe the surrounding structure, the location of the Matrigel deposit is now transformed into a sub–RPE deposit. In animals that lacked photoreceptors, Matrigel fails to induce RPE translocation, suggesting the requirement of a signal from photoreceptors.
Our results support a novel mechanism of sub–RPE deposit formation in which the disruption the PRE–photoreceptors contact by material accumulated in the subretinal space plays a key role. To restore the RPE–photoreceptor contact, RPE cells migrate toward photoreceptors and resume their former relationship. The subretinal material consequently becomes sub–RPE deposit. Our data also provide evidence that a signal from photoreceptors is required to induce trophism of RPE cells and maintain the dynamic nature of the RPE–photoreceptor relationship. Our work therefore represents a step towards understanding of the pathogenesis of AMD.
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