This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.įunding: The research was supported by NIH grant EY05318 and EY015435 to P.D and by the Core grant for Vision Research P30EY14104. Received: JAccepted: OctoPublished: November 3, 2008Ĭopyright: © 2008 Saint-Geniez et al. PLoS ONE 3(11):Įditor: Tailoi Chan-Ling, University of Sydney, Australia (2008) Endogenous VEGF Is Required for Visual Function: Evidence for a Survival Role on Müller Cells and Photoreceptors. Similarly, the addition of exogenous VEGF to freshly isolated photoreceptor cells and outer-nuclear-layer explants demonstrated VEGF to be highly neuroprotective.Ĭitation: Saint-Geniez M, Maharaj ASR, Walshe TE, Tucker BA, Sekiyama E, Kurihara T, et al. siRNA-based suppression of VEGF expression in a Müller cell line in vitro supports the existence of an autocrine role for VEGF in Müller cell survival. By four weeks, the increase in neural cell death was associated with reduced thickness of the inner and outer nuclear layers and a decline in retinal function as measured by electroretinograms. After 14 days of VEGF neutralization, there was no effect on the inner and outer retina vasculature, but a significant increase in apoptosis of cells in the inner and outer nuclear layers. Systemic neutralization of VEGF was accomplished in mice by adenoviral expression of sFlt1. Using immunohistochemistry and Lac-Z reporter mouse lines, we report that VEGF is produced by various cells in the adult mouse retina and that VEGFR2, the primary signaling receptor, is also widely expressed, with strong expression by Müller cells and photoreceptors.
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