June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Pathological Changes in Human Lens Epithelium Gamma-Glutamyl Transpeptidase Expression
Author Affiliations & Notes
  • Margaret Young
    Ophthalmology, University Health, Shreveport, LA, Shreveport, LA
  • Marlyn P Langford
    Ophthalmology, University Health, Shreveport, LA, Shreveport, LA
  • Thomas B Redens
    Ophthalmology, University Health, Shreveport, LA, Shreveport, LA
  • Shubnum Chaudhery
    Pathology, University Health, Shreveport, LA
  • Footnotes
    Commercial Relationships Margaret Young, None; Marlyn Langford, None; Thomas Redens, None; Shubnum Chaudhery, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 5603. doi:
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      Margaret Young, Marlyn P Langford, Thomas B Redens, Shubnum Chaudhery; Pathological Changes in Human Lens Epithelium Gamma-Glutamyl Transpeptidase Expression. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):5603.

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

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Abstract

Purpose: To identify changes in the distribution of gamma-glutamyl transpeptidase (GGT; key enzyme in the recapture of the anti-oxidant glutathione and maintenance of barrier function) in lens of diabetic and non-diabetic human eyes.

Methods: Lens GGT expression in normal mammalian (mouse, rat, rabbit, and monkey) and 8 enucleated human paraffin-embedded eyes (9 to 65 years of age), 6 from diabetic (3 aphakic) and 2 post trauma (1 aphakic) cases, was assessed by immunohistochemical analysis.

Results: Immunoreactive GGT was expressed in the cytoplasm and on the nuclear and cell membranes of the cortical lens epithelial cells. GGT was only expressed by nucleated epithelial cells at the lens equator and along the anterior and posterior lens capsule of normal mammalian and human lens from enucleated eyes. GGT was not expressed by lens fibers or in the lens nucleus. In contrast, GGT was expressed in the cytoplasm and cell membrane (no or weak nuclear membrane expression) of lens epithelial cells undergoing epithelial-mesenchymal transition characteristic of cataract formation and in hypertrophic epithelial cell in lens fragments (5 to 100-fold larger than the normal lens epithelial cell) migrating from the lens capsule. Similarly, cataractous epithelial GGT expression was exhibited by remnant lens epithelial cells within the capsule of aphakic diabetic and non-diabetic eyes.

Conclusions: The results demonstrate changes in the expression and distribution of lenticular GGT in post trauma and diabetic enucleated human eyes. The results suggest onset of pre-cataractous lens pathology is associated with changes in GGT distribution in cortical epithelial cells. These GGT expression changes may affect lens glutathione levels and function.

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