May 2007
Volume 48, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2007
Expression of BCL-2 Family Members Under Glutathione Depletion in the Mouse Retina
Author Affiliations & Notes
  • I. Kim
    Department of Ophthalmology, The Catholic University of Korea, Seoul, Republic of Korea
  • S.-W. Jung
    Department of Ophthalmology, The Catholic University of Korea, Seoul, Republic of Korea
  • M. Park
    Department of Ophthalmology, The Catholic University of Korea, Seoul, Republic of Korea
  • J.-I. Moon
    Department of Ophthalmology, The Catholic University of Korea, Seoul, Republic of Korea
  • Footnotes
    Commercial Relationships I. Kim, None; S. Jung, None; M. Park, None; J. Moon, None.
  • Footnotes
    Support The Basic Research Program of the Korea Science & Engineering Foundation No. R01-2006-000-10488-0
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 5906. doi:
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    • Get Citation

      I. Kim, S.-W. Jung, M. Park, J.-I. Moon; Expression of BCL-2 Family Members Under Glutathione Depletion in the Mouse Retina. Invest. Ophthalmol. Vis. Sci. 2007;48(13):5906.

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

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Abstract

Purpose:: Glutathione (GSH) is known to play a critical role in the cellular defense against unregulated oxidative stress in mammalian cells including neurons. We previously demonstrated that GSH depletion induces cell death in the retina, but the mechanism of cell defense by GSH is still unclear. Thus, we here examined expression of BCL-2 family members (bcl-2, bcl-XL, bax, bak, N-BAK and bad) known to play a key role in determining cell viability.

Methods:: In order to deplete intracellular GSH, we injected buthionine sulphoximine (BSO), an inhibitor of γ-glutamylcysteine synthetase to mice. After 0, 1, 4, and 7 days of BSO injection, total RNAs from each animals were isolated and subjected to real-time RT-RCR analysis.

Results:: Expression of bcl-XL increased one day after BSO injection, but was back to the basal level on day 4. Its expression decreased after 7 days. Expressions of bcl-2 and bax were significantly decreased from 4 days after BSO injection, whereas expression of bad was not changed. An anti-apoptotic molecule, bak displayed a significant decrease 7 days after BSO injection, whereas neuronal cell specific BAK, N-BAK was not altered in its gene expression. Taken together, we demonstrated that glutathione depletion altered expressions of BCL-2 family members in distinct manners. In particular, pro-survival molecule, bcl-2 was decreased under GSH depletion.

Conclusions:: Thus, bcl-2 may play a critical role in GSH-dependent cellular protection in the retina against unregulated oxidative stress, and which implies bcl-2 may provide a potent therapeutic tool for cures against oxidative stress induced retinal degenerative diseases such as glaucoma, retinopathy, and age-related macular degeneration.

Keywords: retina: proximal (bipolar, amacrine, and ganglion cells) • oxidation/oxidative or free radical damage • inner retina dysfunction: biochemistry and cell biology 
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