March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
Glutaredoxin (Grx2) Gene Knockout Suppresses Fiber Cell Differentiation and Delays De-nucleation of the Mouse Lens
Author Affiliations & Notes
  • Marjorie F. Lou
    Veterinary Medicine & Biomedical Sciences, University of Nebraska-Lincoln, Lincoln, Nebraska
    Department of Ophthalmology, University of Nebraska Medical Center, Omaha, Nebraska
  • Subhasree Basu
    Pathology Anatomy & Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania
  • Yibo Yu
    Veterinary Medicine & Biomedical Sciences, University of Nebraska-Lincoln, Lincoln, Nebraska
  • Hongli Wu
    Veterinary Medicine & Biomedical Sciences, University of Nebraska-Lincoln, Lincoln, Nebraska
  • A S. Menko
    Pathology Anatomy & Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania
  • Footnotes
    Commercial Relationships  Marjorie F. Lou, None; Subhasree Basu, None; Yibo Yu, None; Hongli Wu, None; A. S. Menko, None
  • Footnotes
    Support  NIH RO1 EY10595
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 5592. doi:
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      Marjorie F. Lou, Subhasree Basu, Yibo Yu, Hongli Wu, A S. Menko; Glutaredoxin (Grx2) Gene Knockout Suppresses Fiber Cell Differentiation and Delays De-nucleation of the Mouse Lens. Invest. Ophthalmol. Vis. Sci. 2012;53(14):5592.

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

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Abstract

Purpose: : Glutaredoxin 2 (Grx2) is an enzyme with dethiolase and peroxidase activities and is present in the mitochondria where it may protect the organelle from oxidative damage and regulate its redox balances. Recently we developed a global Grx2 gene knockout (KO) mouse model with a phenotype of early age-dependent cataract development, compared with the wild type (WT) control. The purpose of this study is to examine how Grx2 gene deletion affects lens development and influence its transparency.

Methods: : Histological slides were made using whole eye globe (5 m WT, Grx2 KO), fixed and sectioned into 5 micron thickness, followed with hematoxylin and eosin staining. Lens cryosections prepared from WT and Grx2 KO mice at 1.2 m were immunostained with the lens differentiation marker filensin, counterstained for F-actin (fluorescent-conjugated phalloidin) and nuclei (TO-PRO-3), and imaged by confocal microscopy. Filensin expression also was examined in 1, 7, and 16 m WT and KO mice by Western blot analysis.

Results: : Lenses from Grx2 null mice showed similar growth in size and weight as WT mice but developed nuclear opacity 3 months sooner than the age-matched control. Histological section at the polar region of the Grx2 KO lens (5 m) showed heavy nuclei staining deep into the fiber cell layers. Saggital cryosections of 1.2 m-old Grx2-/- mice stained for F-actin showed a normal anterior-posterior alignment of fiber cells in the lens cortex, but cross-sectional analysis revealed patches of aberrant organization of the normal hexagonal packed structure. Immunostaining showed a lower-level expression of filensin in the cortex of Grx2-/- lenses compared to controls that was confirmed by Western blot analysis. And, unlike control lenses in which nuclei are lost with fiber cell differentiation, in the Grx2-/- lens nuclei persisted in the centermost fiber cells.

Conclusions: : Grx2 gene deletion interferes the lens fiber differentiation and also inhibits the process of de-nucleation during lens development. Aberration of both may contribute to the early nuclear cataract formation in the Grx2-/- lens.

Keywords: transgenics/knock-outs • differentiation • cataract 
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