Deletion of GLUT1 in Mouse Lens Epithelium Leads to Cataract Formation

Aditi Swarup, Brent A Bell, Jianhai Du, John Y S Han, Jamie Soto, E Dale Abel, Arturo Bravo Nuevo, Paul G FitzGerald, Neal S Peachey, Nancy J Philp

Research output: Contribution to journalArticlepeer-review

Abstract

The primary energy substrate of the lens is glucose and uptake of glucose from the aqueous humor is dependent on glucose transporters. GLUT1, the facilitated glucose transporter encoded by Slc2a1 is expressed in the epithelium of bovine, human and rat lenses. In the current study, we examined the expression of GLUT1 in the mouse lens and determined its role in maintaining lens transparency by studying effects of postnatal deletion of Slc2a1. In situ hybridization and immunofluorescence labeling were used to determine the expression and subcellular distribution of GLUT1 in the lens. Slc2a1 was knocked out of the lens epithelium by crossing transgenic mice expressing Cre recombinase under control of the GFAP promoter with Slc2a1

Original languageAmerican English
JournalExperimental eye research
Volume17
StatePublished - Mar 28 2018

Keywords

  • Cataract
  • GFAP-Cre(+/0)
  • Glut1
  • Lens
  • LensΔGlut1: Slc2a1(loxP/loxP)
  • LensΔGlut1Het: Slc2a1(loxP/+)
  • Optical Coherence Tomography
  • Optical coherence tomography
  • SD-OCT
  • Slc2a1

Disciplines

  • Medicine and Health Sciences

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