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Gary E. Korte, PhD
Bronx, NY

Arch Ophthalmol. 1986;104(6):802-804.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—The recent reports on the interactions between retinal pigment epithelium (RPE) and endothelium in vitro point out that an RPElocated inhibitor of neovascularization and an endothelium-located chemoattractant for RPE cells explain only part of the story of how neovascularization and the status quo at Bruch's membrane are controlled.^1,2 I would like to point out the following evidence derived from experimental animals and human pathologic studies that suggest interesting and relevant interactions between RPE and endothelium in vivo.

Animal experiments have shown that choriocapillaris atrophies (its endothelium thickens and loses its fenestrae; endothelial cells die, and the capillary plexus retracts) when and where RPE is destroyed. This is seen, for example, in rabbits that receive sodium iodate intravenously.³ The chemical destroys the RPE in a patchy manner. Choriocapillary atrophy ensues at sites of RPE loss—and only there.

In histologic studies of human eyes with RPE degeneration . . . [Full Text PDF of this Article]

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