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Journal of Ophthalmology
Volume 2015 (2015), Article ID 369312, 9 pages
http://dx.doi.org/10.1155/2015/369312
Research Article

Responses of Multipotent Retinal Stem Cells to IL-1β, IL-18, or IL-17

1Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
2Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou 510060, China
3Histology Core, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
4Stowers Institute for Medical Research, Kansas City, MO 64110, USA
5Department of Anatomy and Cell Biology, University of Kansas School of Medicine, Kansas City, KS 66160, USA

Received 29 March 2015; Accepted 14 July 2015

Academic Editor: Naoshi Kondo

Copyright © 2015 Shida Chen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Purpose. To investigate how multipotent retinal stem cells (RSCs) isolated from mice respond to the proinflammatory signaling molecules, IL-1β, IL-18, and IL-17A. Materials and Methods. RSCs were cultured in a specific culture medium and were treated with these cytokines. Cell viability was detected by MTT assay; ultrastructure was evaluated by transmission electron microscopy; expression of IL-17rc and proapoptotic proteins was detected by immunocytochemistry and expression of Il-6 and Il-17a was detected by quantitative RT-PCR. As a comparison, primary mouse retinal pigment epithelium (RPE) cells were also treated with IL-1β, IL-18, or IL-17A and analyzed for the expression of Il-6 and Il-17rc. Results. Treatment with IL-1β, IL-18, or IL-17A decreased RSC viability in a dose-dependent fashion and led to damage in cellular ultrastructure including pyroptotic and/or necroptotic cells. IL-1β and IL-18 could induce proapoptotic protein expression. All treatments induced significantly higher expression of Il-6 and Il-17rc in both cells. However, neither IL-1β nor IL-18 could induce Il-17a expression in RSCs. Conclusions. IL-1β, IL-18, and IL-17A induce retinal cell death via pyroptosis/necroptosis and apoptosis. They also provoke proinflammatory responses in RSCs. Though IL-1β and IL-18 could not induce Il-17a expression in RSCs, they both increase Il-17rc expression, which may mediate the effect of Il-17a.