July 2018
Volume 59, Issue 9
ARVO Annual Meeting Abstract  |   July 2018
Mitochondrial integrity and function in hPSC-derived RPE
Author Affiliations & Notes
  • Divya Sinha
    Waisman Center, University of Wisconsin-Madison, Madison, Wisconsin, United States
    McPherson Eye Research Institute, University of Wisconsin-Madison, Madison, Wisconsin, United States
  • Footnotes
    Commercial Relationships   Divya Sinha, None
  • Footnotes
    Support  Research to Prevent Blindness Catalyst Award, International Retina Research Foundation, Foundation Fighting Blindness, NIH R01EY024588, Retinal Research Foundation Emmett A. Humble Distinguished Directorship, McPherson Eye Research Institute (Sandra Lemke Trout Chair), Carl and Mildred Reeves Foundation, NIH P30HD03352, Muskingum County Community Foundation, SIG 1S10OD018039-01 for Seahorse XFe96 analyzer, Support Grant P30 CA014520 to SMSSF (core service of the University of Wisconsin Carbone Cancer Center)
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 1611. doi:
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      Divya Sinha; Mitochondrial integrity and function in hPSC-derived RPE. Invest. Ophthalmol. Vis. Sci. 2018;59(9):1611.

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

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Presentation Description :
Retinal pigment epithelium (RPE), a highly metabolically active monolayer of cells performing critical functions in the outer retina, is lost in several retinal degenerative disorders including age-related macular degeneration (AMD). Efforts are underway to develop transplantation strategies utilizing human pluripotent stem cell-derived RPE (hPSC-RPE) to replace these cells. RPE cells are known to be rich in mitochondria, however, the metabolic state of in vitro differentiated hPSC-RPE cells and their response to patient-specific in vivo stressors is not known. We investigated the mitochondrial integrity and function of these cells under baseline condition and conditions targeting mitochondrial respiration. Our results show that hPSC-RPE cells have healthy mitochondrial function, which can be affected by exposure to certain treatments. More specifically, the spare respiratory capacity (SRC), which is an indicator of a cell’s ability to manage cellular stress, can be modulated. This information has implications not only for cell survival and function post-transplantation but also in understanding and targeting mitochondrial function in early stages of disease.

This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.


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