June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Damage to the corneal endothelial cell in situ is attenuated by long wave red light
Author Affiliations & Notes
  • Claudia Núñez-Álvarez
    Neurobiology of the Retina, Ophthalmologic Research Foundation FIO, Oviedo, Spain
  • Susana del Olmo Aguado
    Neurobiology of the Retina, Ophthalmologic Research Foundation FIO, Oviedo, Spain
  • Jesús Merayo-Lloves
    Ocular Surface, Ophtalmologic Research Foundation FIO, Oviedo, Spain
  • Neville N Osborne
    Neurobiology of the Retina, Ophthalmologic Research Foundation FIO, Oviedo, Spain
  • Footnotes
    Commercial Relationships Claudia Núñez-Álvarez, None; Susana Olmo Aguado, None; Jesús Merayo-Lloves, None; Neville Osborne, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 5733. doi:
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      Claudia Núñez-Álvarez, Susana del Olmo Aguado, Jesús Merayo-Lloves, Neville N Osborne, Neurobiology of the Retina; Damage to the corneal endothelial cell in situ is attenuated by long wave red light. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):5733.

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

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Abstract

Purpose: To determine whether the damaging influence of raised IOP to corneal endothelial cells in the rat is blunted by treatment with red light.

Methods: Corneal endothelial cells from one eye in anesthetised rats were damaged by placing a needle in the anterior chamber and elevating the intraocular pressure (IOP, approximately 130mm Hg) for 60 minutes in the dark. In some instances the cornea was exposed to red light (3000 lux, 625-635nm). Rats were either killed immediately or after periods of up to 3 days. Flat mounts and transverse sections of cornea were processed for the localisation of tight junctional protein ZO-1 and JC-1 to monitor mitochondrial health with their degree of depolarization indicated by changes in the red to green intensity of fluorescence.

Results: Raise IOP causes damage to the mosaic appearance of corneal endothelial cells clearly indicated by staining for ZO-1. Exposure to red light during elevation of IOP reduced the amount of patchy damage to endothelial cells. Corneal endothelial cells appear green when stained with JC-1 but after 60 minutes of raised IOP the cytoplasm of many cells appear red. Both the numbers and intensity of red endothelial cells increased in JC-1 stained corneas exposed to red light. Three days after an insult of raised IOP, some red JC-1 staining was present only in corneas exposed to red light.

Conclusions: Raised IOP causes damage and disruption of corneal endothelial cells. This process is blunted by red light. JC-1 staining suggests that endothelial cell mitochondria are activated by raised IOP (presumably as a protective mechanism) and that this process is enhanced by red light.

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