Iron is neurotoxic in retinal detachment and transferrin confers neuroprotection
Alejandra Daruich1,2,3, Quentin Le Rouzic1, Laurent Jonet1, Marie-Christine Naud1, Laura Kowalczuk2, Jean-Antoine Pournaras2, Jeffrey H. Boatright4,5, Aurélien Thomas6,7, Natacha Turck7,8, Alexandre Moulin2, Francine Behar-Cohen1,7,9,*,† and Emilie
Picard1,*
NEUROSCIENCE
Science Advances 09 Jan 2019:
Vol. 5, no. 1, eaau9940
DOI: 10.1126/sciadv.aau9940

Abstract
In retinal detachment (RD), photoreceptor death and permanent vision loss are caused by neurosensory retina separating from the retinal pigment epithelium because of subretinal fluid (SRF), and successful surgical reattachment is not predictive of total
visual recovery. As retinal iron overload exacerbates cell death in retinal diseases, we assessed iron as a predictive marker and therapeutic target for RD. In the vitreous and SRF from patients with RD, we measured increased iron and transferrin (TF)
saturation that is correlated with poor visual recovery. In ex vivo and in vivo RD models, iron induces immediate necrosis and delayed apoptosis. We demonstrate that TF decreases both apoptosis and necroptosis induced by RD, and using RNA sequencing,
pathways mediating the neuroprotective effects of TF are identified. Since toxic iron accumulates in RD, we propose TF supplementation as an adjunctive therapy to surgery for improving the visual outcomes of patients with RD.

http://advances.sciencemag.org/content/5/1/eaau9940?rss=1

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