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Increased O-GlcNAc causes disrupted lens fiber cell differentiation and cataracts

Kai Wang1, Shiuh-Rong Ho, Weiming Mao

  • 1Department of Medicine, Division of Endocrinology, Diabetes and metabolism, University of Alabama at Birmingham, 1808 7th Avenue South, Birmingham, AL 35294, USA.

Biochemical and Biophysical Research Communications
|July 7, 2009
PubMed

Insights

Elevated O-GlcNAc levels in the eye lens inhibit proteasome function, leading to cataract formation. This study demonstrates a direct link between O-GlcNAc, proteasome inhibition, and cataracts in mice.

Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Biochemistry

Background:

  • Cataract formation is linked to reduced lens proteolytic activity.
  • O-linked N-acetylglucosamine (O-GlcNAc) is an endogenous proteasome inhibitor.
  • A potential link exists between lens O-GlcNAc levels, proteasome function, and cataractogenesis.

Purpose of the Study:

  • To investigate the causal relationship between O-GlcNAc, proteasome inhibition, and cataract development in the eye lens.
  • To establish and utilize transgenic mouse models for studying O-GlcNAc's role in the lens.

Main Methods:

  • Developed transgenic mice overexpressing a dominant-negative O-GlcNAcase (GK-NCOAT) in the lens.
  • Measured O-GlcNAc levels and proteasome activity in transgenic mouse lenses.
  • Assessed cataract formation and lens fiber cell denucleation in experimental and control mice.

Main Results:

  • Transgenic mice exhibited significantly increased O-GlcNAc levels in their lenses.
  • Proteasome function was decreased in the lenses of transgenic mice.
  • Transgenic mice developed larger cataracts, and lens fiber cell denucleation was inhibited compared to controls.

Conclusions:

  • Increased O-GlcNAc in the lens inhibits proteasome function, contributing to cataract formation.
  • Inhibition of proteasome function by O-GlcNAc may attenuate lens fiber cell denucleation.
  • These findings provide a molecular explanation for cataracts as a complication of diabetes, given O-GlcNAc's glucose dependency.

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