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Mol. Cells 2013; 35(3): 235-242

Published online March 31, 2013

https://doi.org/10.1007/s10059-013-2276-y

© The Korean Society for Molecular and Cellular Biology

Differential Cell Death and Bcl-2 Expression in the Mouse Retina after Glutathione Decrease by Systemic D,L-Buthionine Sulphoximine Administration

Myoung Hee Park, So Yeun Kim, Chanil Moon, Young Chul Bae, Jung-Il Moon, and Cheil Moon

Department of Brain Science, Graduate School, Daegu Gyeongbuk Institute of Science and Technology, Daegu 711-873, Korea, Department of Ophthalmology, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea, Department of Oral Anatomy and Neurobiology, School of Dentistry, Kyungpook National University, Daegu 700-412, Korea, 4Department of Cardiology, School of Medicine, Hanyang University, Seoul 133-791, Korea

Received: October 22, 2013; Revised: December 17, 2013; Accepted: December 26, 2013

Abstract

Glutathione (GSH) plays a critical role in cellular defense against unregulated oxidative stress in mammalian cells including neurons. We previously demonstrated that GSH decrease using [D, L]-buthionine sulphoximine (BSO) induces retinal cell death, but the underlying mechanisms of this are still unclear. Here, we demonstrated that retinal GSH level is closely related to retinal cell death as well as expression of an anti-apoptotic molecule, Bcl-2, in the retina. We induced differential expression of retinal GSH by single and multiple administrations of BSO, and examined retinal GSH levels and retinal cell death in vivo. Single BSO administration showed a transient decrease in the retinal GSH level, whereas multiple BSO administration showed a persistent decrease in the retinal GSH level. Retinal cell death also showed similar patterns: transient increases of retinal cell death were observed after single BSO administration, whereas persistent increases of retinal cell death were observed after multiple BSO administration. Changes in the retinal GSH level affected Bcl-2 expression in the retina. Immunoblot and immunohistochemical analyses showed that single and multiple administration of BSO induced differential expressions of Bcl-2 in the retina. Taken together, the results of our study suggest that the retinal GSH is important for the survival of retinal cells, and retinal GSH appears to be deeply related to Bcl-2 expression in the retina. Thus, alteration of Bcl-2 expression may provide a therapeutic tool for retinal degenerative diseases caused by retinal oxidative stress such as glaucoma or retinopathy.

Keywords Bcl-2, BSO, glutathione, oxidative stress, retina

Article

Research Article

Mol. Cells 2013; 35(3): 235-242

Published online March 31, 2013 https://doi.org/10.1007/s10059-013-2276-y

Copyright © The Korean Society for Molecular and Cellular Biology.

Differential Cell Death and Bcl-2 Expression in the Mouse Retina after Glutathione Decrease by Systemic D,L-Buthionine Sulphoximine Administration

Myoung Hee Park, So Yeun Kim, Chanil Moon, Young Chul Bae, Jung-Il Moon, and Cheil Moon

Department of Brain Science, Graduate School, Daegu Gyeongbuk Institute of Science and Technology, Daegu 711-873, Korea, Department of Ophthalmology, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea, Department of Oral Anatomy and Neurobiology, School of Dentistry, Kyungpook National University, Daegu 700-412, Korea, 4Department of Cardiology, School of Medicine, Hanyang University, Seoul 133-791, Korea

Received: October 22, 2013; Revised: December 17, 2013; Accepted: December 26, 2013

Abstract

Glutathione (GSH) plays a critical role in cellular defense against unregulated oxidative stress in mammalian cells including neurons. We previously demonstrated that GSH decrease using [D, L]-buthionine sulphoximine (BSO) induces retinal cell death, but the underlying mechanisms of this are still unclear. Here, we demonstrated that retinal GSH level is closely related to retinal cell death as well as expression of an anti-apoptotic molecule, Bcl-2, in the retina. We induced differential expression of retinal GSH by single and multiple administrations of BSO, and examined retinal GSH levels and retinal cell death in vivo. Single BSO administration showed a transient decrease in the retinal GSH level, whereas multiple BSO administration showed a persistent decrease in the retinal GSH level. Retinal cell death also showed similar patterns: transient increases of retinal cell death were observed after single BSO administration, whereas persistent increases of retinal cell death were observed after multiple BSO administration. Changes in the retinal GSH level affected Bcl-2 expression in the retina. Immunoblot and immunohistochemical analyses showed that single and multiple administration of BSO induced differential expressions of Bcl-2 in the retina. Taken together, the results of our study suggest that the retinal GSH is important for the survival of retinal cells, and retinal GSH appears to be deeply related to Bcl-2 expression in the retina. Thus, alteration of Bcl-2 expression may provide a therapeutic tool for retinal degenerative diseases caused by retinal oxidative stress such as glaucoma or retinopathy.

Keywords: Bcl-2, BSO, glutathione, oxidative stress, retina

Mol. Cells
Nov 30, 2022 Vol.45 No.11, pp. 763~867
COVER PICTURE
Naive (cyan) and axotomized (magenta) retinal ganglion cell axons in Xenopus tropicalis (Choi et al., pp. 846-854).

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