April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
TSG-6 protects corneal endothelium from trans-corneal freezing injury in rabbits
Author Affiliations & Notes
  • Jeong-Ah Kim
    Ophthalmology, Seoul National University Hospital, Seoul, Republic of Korea
  • Joo Youn Oh
    Ophthalmology, Seoul National University Hospital, Seoul, Republic of Korea
    Laboratory for Ocular Regenerative Medicine and Immunology, Biomedical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 2033. doi:
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      Jeong-Ah Kim, Joo Youn Oh; TSG-6 protects corneal endothelium from trans-corneal freezing injury in rabbits. Invest. Ophthalmol. Vis. Sci. 2014;55(13):2033.

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

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Abstract

Purpose: To investigate whether an anti-inflammatory protein TNF-α stimulated gene/protein 6 (TSG-6) or an anti-apoptotic protein stanniocalcin-1 (STC-1) might have protective effects on corneal endothelial cells in rabbits with transcorneal freezing injury.

Methods: Trans-corneal freezing (-80°C, 30 sec) was applied to the corneal surface in New Zealand White rabbits, and either TSG-6(10 μg/100 μl) or STC-1 (10 μg/100 μl) was injected into the anterior chamber right after the injury. The same volume of balanced salt solution (BSS) was injected in control group. Corneas were examined for development of opacity and recorded by photography every 2 or 6 hours during 48 hours post-injury. Corneal thickness, endothelial cell count, and hexagonality of endothelial cells were also measured using pachymeter and specular microscope. Forty eight hours after injury, the animals were humanely killed, and the corneas were subjected to vital staining with alizarin red and trypan blue.

Results: TSG-6 significantly decreased the development of corneal opacity and edema after injury, compared to BSS- or STC-1. The rise in corneal thickness after injury was significantly reduced in TSG-6-treated eyes, and the number of corneal endothelial cells and hexagonality were markedly preserved by TSG-6. However, there were no differences in corneal thickness and endothelial cell counts between BSS- and STC-1-treated eyes. Vital staining showed that there were fewer number of trypan blue-stained dead cells in corneal endothelium of TSG-6-treated eyes than BSS-treated controls.

Conclusions: Results demonstrated that TSG-6 protected corneal endothelial cells from transcorneal freezing injury. Given that TSG-6 is an anti-inflammatory protein, data also suggest that inflammation might be responsible for endothelial damage in freezing injury to the cornea, and modulation of inflammation would be beneficial for protecting corneal endothelial cells.

Keywords: 481 cornea: endothelium • 426 apoptosis/cell death • 480 cornea: basic science  
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