May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Involvement of Egr–1 in lens epithelial cell death induced by selenite.
Author Affiliations & Notes
  • T. Nakajima
    Senju Lab., Senju Pharmaceutical Co., Ltd., Beaverton, OR
  • P.B. Belusko
    Senju Lab., Senju Pharmaceutical Co., Ltd., Beaverton, OR
  • R.D. Walkup
    Senju Lab., Senju Pharmaceutical Co., Ltd., Beaverton, OR
  • M. Azuma
    Senju Lab., Senju Pharmaceutical Co., Ltd., Beaverton, OR
  • T.R. Shearer
    Department of Integrative Biosciences, Oregon Health & Science University, Portland, OR
  • Footnotes
    Commercial Relationships  T. Nakajima, Senju Pharmaceutical Co., Ltd. E; P.B. Belusko, Senju Pharmaceutical Co., Ltd. E; R.D. Walkup, Senju Pharmaceutical Co., Ltd. E; M. Azuma, Senju Pharmaceutical Co., Ltd. E; T.R. Shearer, Oregon Health & Science University C.
  • Footnotes
    Support  EY03600
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 2646. doi:
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      T. Nakajima, P.B. Belusko, R.D. Walkup, M. Azuma, T.R. Shearer; Involvement of Egr–1 in lens epithelial cell death induced by selenite. . Invest. Ophthalmol. Vis. Sci. 2004;45(13):2646.

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

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Abstract

Abstract: : Purpose: Selenite cataract is believed to be caused by an initial insult to rat lens epithelial cells. Micro array analysis indicated that expression of mRNA for early growth response protein–1 (Egr–1) was significantly increased. The functions of Egr–1 include induction of apoptosis, and suppression of growth and transformation. The purpose of the present experiment was to clarify the involvement of Egr–1 in lens epithelial cell death induced by selenite. Methods: Mouse lens epithelial cells α–TN4 cells were cultured with selenite. Leakage of lactate dehydrogenase (LDH) from the cells into the medium was used as a marker for cell death. Changes in the expression of mRNA and protein for Egr–1 were confirmed by RT–PCR and immunoblotting. Treatment of cells with antisense oligonucleotide for Egr–1 was used to confirm the involvement of Egr–1 in lens epithelial cell death induced by selenite. Results: When α–TN4 cells were cultured with selenite, leakage of LDH into the medium, expression of mRNA for Egr–1, and expression of Egr–1 protein were increased. Antisense oligonucleotide for Egr–1 significantly diminished leakage of LDH. Conclusions: These results suggested that increased activity of Egr–1 is a factor in lens epithelial cell death induced by selenite, leading to cataract formation.

Keywords: cell death/apoptosis • gene/expression • cataract 
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