July 2018
Volume 59, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2018
Effect of diabetes mellitus on corneal crystallins
Author Affiliations & Notes
  • Judy Weng
    Chapman University School of Pharmacy, Irvine, California, United States
  • Ashley Barbarino
    Chapman University School of Pharmacy, Irvine, California, United States
  • Ajay Sharma
    Chapman University School of Pharmacy, Irvine, California, United States
  • Footnotes
    Commercial Relationships   Judy Weng, None; Ashley Barbarino, None; Ajay Sharma, None
  • Footnotes
    Support  Chapman University School of Pharmacy Start up fund
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 3301. doi:
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      Judy Weng, Ashley Barbarino, Ajay Sharma; Effect of diabetes mellitus on corneal crystallins. Invest. Ophthalmol. Vis. Sci. 2018;59(9):3301.

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

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Abstract

Purpose : Recent clinical data demonstrates that diabetic patients suffer from disproportionately high incidence of dry eye. Corneal epithelial cells play a vital role in keeping the ocular surface hydrated. Corneal epithelial cells have been shown to express abundant amount of water-soluble proteins collectively termed as corneal crystallins. In addition to their proposed function of affecting light scattering in the cornea, these crystallins have been shown to protect the corneal epithelial cells from oxidative damage or apoptosis. The present study investigates the effect of diabetes mellitus on the expression of three corneal crystallins: aldehyde dehydrogenase (ALDH)3A1, ALDH1A1 and transketolase (TKT).

Methods : Mouse models of type I and type II diabetes were used in the study. Type I diabetes was induced in C57 mice by single intraperitoneal injection of streptozotocin (STZ). For type II diabetes, db/db mouse model was used. Blood glucose was quantified using tail clip method. Tear secretion was quantified using phenol red thread test. The corneas were harvested at 8 weeks after induction of diabetes mellitus in STZ-injected mice and after 8 weeks of hyperglycemia onset in the db/db mice. The corneas harvested from age matched nondiabetic mice were used as controls. The corneas were processed for RNA isolation, cDNA preparation and quantification of ALDH3A1, ALDH1A1 and TKT gene expression. For in vitro experiments, the human corneal epithelial cells were exposed to high glucose for various time points. The RNA was isolated from high glucose exposed and control cells for cDNA preparation and quantification of ALDH3A1, ALDH1A1 and TKT gene expression.

Results : Our data demonstrated that both type I and type II diabetes caused a significant decrease in the gene expression of corneal crystallins after 8 weeks of persistent hyperglycemia. A concurrent reduction in the tear secretion was also noted in both the animal models. The level of hyperglycemia was more severe in the type I diabetes STZ mouse model compared to the type II diabetes db/db mouse model but the decrease in the corneal crystallins gene expression was similar in both the animal models. In vitro exposure of corneal human epithelial cells to high glucose also caused a decrease in the gene expression of corneal crystallins.

Conclusions : Diabetes mellitus-associated hyperglycemia causes a significant decrease in the expression of corneal crystallins.

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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