September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Retinal endothelin-2 is necessary for stress-induced retinal neuroprotection
Author Affiliations & Notes
  • Marcus Hooper
    Genetics, University of Florida, Gainesville, Florida, United States
  • John Ash
    Genetics, University of Florida, Gainesville, Florida, United States
  • Footnotes
    Commercial Relationships   Marcus Hooper, None; John Ash, None
  • Footnotes
    Support  NIH R01EY016459-10
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 4390. doi:
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      Marcus Hooper, John Ash; Retinal endothelin-2 is necessary for stress-induced retinal neuroprotection
      . Invest. Ophthalmol. Vis. Sci. 2016;57(12):4390.

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

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Purpose : Retinal degeneration is a gradual process, but would proceed much more quickly in the absence of potent endogenous neuroprotective pathways. We study these pathways for the long-term goal of treating neurodegenerative diseases. Endothelin-2 (edn2) is a cytokine that is highly induced under conditions of retinal stress and degeneration. Edn2 is photoreceptor-derived and has been proposed to signal to glial cells during stress. We set out to determine whether edn2 and its receptor, endothelin receptor A (ednrA), are necessary for stress-induced photoreceptor protection using the light damage model.

Methods : For preconditioning (PC), mice were exposed to cyclic bright light for 6 days at 400 lux. For light damage (LD), mice were exposed to 1300 lux for 4 hours. Retinal photoreceptor function and a-wave amplitudes were determined by scotopic electroretinography (ERG). Outer nuclear layer (ONL) thickness was measured by Spectral Domain-Optical Coherence Tomography (OCT). Immunohistochemistry was used to examine glial fibrillary acidic protein (GFAP) expression. Quantitative PCR (qPCR) was used to measure mRNA levels. All procedures involving animals were conducted in accordance with the ARVO Statement for the Use of Animals in Ophthalmic and Vision Research.

Results : Our data demonstrate that edn2 is required for PC-induced protection from LD. Retinal edn2 or ednrA knockout mice have ONL thinning and reduced ERG a-wave amplitudes following exposure to PC and LD. Additionally, retinal edn2 knockout mice have reduced GFAP expression in light stress, which suggests that the Müller cell stress response may be dependent on edn2.

Conclusions : Retinal edn2 and ednrA are necessary for stress-induced neuroprotection using the light damage model. Retinal edn2 knockout mice have defective upregulation of GFAP in Müller cells. It may be that edn2 is involved in regulating the Müller glial response to stress. As such, future questions are centered on whether other Müller cell functions are regulated by edn2.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.


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