June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Role of choroid endothelial cells in the homeostasis of the outer retina
Author Affiliations & Notes
  • Enrique J. Rodriguez-Boulan
    Opthalmology-Margaret Dyson Vision Research Institute, Weill Cornell Medical College, New York, New York, United States
  • Footnotes
    Commercial Relationships   Enrique Rodriguez-Boulan, None
  • Footnotes
    Support  NIH grant EY08538; Tri-Institutional Stem Cell Initiative TRISCI2013-028
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 4731. doi:
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      Enrique J. Rodriguez-Boulan; Role of choroid endothelial cells in the homeostasis of the outer retina. Invest. Ophthalmol. Vis. Sci. 2017;58(8):4731.

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      © ARVO (1962-2015); The Authors (2016-present)

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Presentation Description : Beyond their role as blood conduits, endothelial cells (ECs) are organ-specific and secrete key angiocrine factors essential for organ differentiation and regeneration. We hypothesized that choroid ECs may regulate the maturation and homeostasis of the outer retina, and that functional defects of choroid ECs could be highly significant for the etiology and pathogenesis of age-related macular degeneration (AMD). We carried out a series of RNAseq analyses to study the changes in gene expression of mouse choroid ECs during retinal terminal differentiation, and to compare the transcriptome of ECs from adult choroid and other tissues. These studies, along with in vitro co-culture assays, the use of reporter mouse models and the generation of EC-specific knockout mice, support the notion that factors secreted by choroid ECs regulate retinal pigment epithelium (RPE) barrier function and the maintenance of adult choroid homeostasis and visual function in response to injury. We also identified a signaling loop involving the Hedgehog pathway between choroid ECs and a population of mesenchymal stem cell (MSC)-like choroidal perivascular cells, recently discovered in our laboratory. Crosstalk between RPE, choroid ECs and MSC-like cells may be key for such processes, and its disruption may contribute to the onset and pathogenesis of AMD.
Ignacio Benedicto1*, Guillermo L. Lehmann1*, Michael Ginsberg2, Daniel J. Nolan2, Rohan Bareja3, Olivier Elemento3, Nazia M. Alam3,4, Glen T. Prusky3,4, Pierre Llanos5, Sina Y. Rabbany5, Arvydas Maminishkis6, Sheldon S. Miller6, Alexandre Wojcinski7, Alexandra L. Joyner7, Shahin Rafii2,8,9, Enrique Rodriguez-Boulan1
*, equal contribution
1. Margaret Dyson Vision Research Institute, Department of Ophthalmology, Weill Cornell Medical College, New York, NY, USA; 2. Angiocrine Bioscience, Inc.; 3. Department of Physiology and Biophysics, Weill Cornell Medical College, New York, NY, USA; 4. Burke Medical Research Institute, White Plains, NY, USA; 5. Bioengineering Program, Hofstra University, Hempstead, NY, USA; 6. Section of Epithelial and Retinal Physiology and Disease, National Eye Institute, National Institutes of Health, Bethesda, MD, USA; 7. Memorial Sloan Kettering Cancer Center, New York, NY, USA; 8. Genetic Medicine, Weill Cornell Medical College, New York, NY, USA; 9. Ansary Stem Cell Institute, Weill Cornell Medical College, New York, NY, USA.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.


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