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Caspase inhibitors protect against NMDA-mediated retinal ganglion cell death

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Caspase inhibitors protect against NMDA-mediated retinal ganglion cell death. / Schuettauf, Frank; Stein, Thomas; Choragiewicz, Tomasz J; Rejdak, Robert; Bolz, Sylvia; Zurakowski, David; Varde, Meghana A; Laties, Alan M; Thaler, Sebastian.

in: CLIN EXP OPHTHALMOL, Jahrgang 39, Nr. 6, 08.2011, S. 545-54.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Schuettauf, F, Stein, T, Choragiewicz, TJ, Rejdak, R, Bolz, S, Zurakowski, D, Varde, MA, Laties, AM & Thaler, S 2011, 'Caspase inhibitors protect against NMDA-mediated retinal ganglion cell death', CLIN EXP OPHTHALMOL, Jg. 39, Nr. 6, S. 545-54. https://doi.org/10.1111/j.1442-9071.2010.02486.x

APA

Schuettauf, F., Stein, T., Choragiewicz, T. J., Rejdak, R., Bolz, S., Zurakowski, D., Varde, M. A., Laties, A. M., & Thaler, S. (2011). Caspase inhibitors protect against NMDA-mediated retinal ganglion cell death. CLIN EXP OPHTHALMOL, 39(6), 545-54. https://doi.org/10.1111/j.1442-9071.2010.02486.x

Vancouver

Schuettauf F, Stein T, Choragiewicz TJ, Rejdak R, Bolz S, Zurakowski D et al. Caspase inhibitors protect against NMDA-mediated retinal ganglion cell death. CLIN EXP OPHTHALMOL. 2011 Aug;39(6):545-54. https://doi.org/10.1111/j.1442-9071.2010.02486.x

Bibtex

@article{c331ce93aaa84eeabdc16fb2b5300759,
title = "Caspase inhibitors protect against NMDA-mediated retinal ganglion cell death",
abstract = "BACKGROUND: Apoptosis is a major mechanism of cell death in glutamate-induced excitotoxicity and caspases as the executors of apoptosis play an important role in the development of various central nervous system and eye diseases. We studied the involvement of certain caspases in excitotoxic retinal ganglion cell death, which was experimentally induced in Brown Norway Rats by application of the glutamate receptor agonist N-methyl-D-aspartate (NMDA).METHODS: Animals were injected intravitreally with one of six caspase inhibitors (against caspases 1, 3, 4, 6, 8 and 9). Seven hours later, NMDA or phosphate-buffered saline as a control was injected intravitreally into the respective eyes. The neuroprotective potential against NMDA toxicity was assessed by retinal ganglion cell quantification. Additionally, wholemount TUNEL was performed.RESULTS: Statistical analysis revealed significant neuroprotective effects for the inhibitors of caspases 3, 6, 8 and 9, but not for those of caspases 1 and 4. The inhibitors of caspases 6 and 9 showed greater neuroprotective potential than those of caspases 3 and 8, although cell death was not entirely averted in any case. Results of ganglion cell counts were confirmed for the most pronounced treatment groups using wholemount TUNEL.CONCLUSION: Excitotoxic retinal ganglion cell death after NMDA injection is mediated mainly through apoptosis, whereby extrinsic as well as intrinsic pathways of caspase activation play a role.",
keywords = "Animals, Apoptosis/drug effects, Caspase Inhibitors, Cell Count, Cell Survival, Cytoprotection, Enzyme Inhibitors/pharmacology, Excitatory Amino Acid Agonists/toxicity, Female, In Situ Nick-End Labeling, Intravitreal Injections, N-Methylaspartate/toxicity, Rats, Rats, Inbred BN, Rats, Long-Evans, Retinal Ganglion Cells/drug effects",
author = "Frank Schuettauf and Thomas Stein and Choragiewicz, {Tomasz J} and Robert Rejdak and Sylvia Bolz and David Zurakowski and Varde, {Meghana A} and Laties, {Alan M} and Sebastian Thaler",
note = "{\textcopyright} 2011 The Authors. Clinical and Experimental Ophthalmology {\textcopyright} 2011 Royal Australian and New Zealand College of Ophthalmologists.",
year = "2011",
month = aug,
doi = "10.1111/j.1442-9071.2010.02486.x",
language = "English",
volume = "39",
pages = "545--54",
journal = "CLIN EXP OPHTHALMOL",
issn = "1442-6404",
publisher = "Wiley-Blackwell",
number = "6",

}

RIS

TY - JOUR

T1 - Caspase inhibitors protect against NMDA-mediated retinal ganglion cell death

AU - Schuettauf, Frank

AU - Stein, Thomas

AU - Choragiewicz, Tomasz J

AU - Rejdak, Robert

AU - Bolz, Sylvia

AU - Zurakowski, David

AU - Varde, Meghana A

AU - Laties, Alan M

AU - Thaler, Sebastian

N1 - © 2011 The Authors. Clinical and Experimental Ophthalmology © 2011 Royal Australian and New Zealand College of Ophthalmologists.

PY - 2011/8

Y1 - 2011/8

N2 - BACKGROUND: Apoptosis is a major mechanism of cell death in glutamate-induced excitotoxicity and caspases as the executors of apoptosis play an important role in the development of various central nervous system and eye diseases. We studied the involvement of certain caspases in excitotoxic retinal ganglion cell death, which was experimentally induced in Brown Norway Rats by application of the glutamate receptor agonist N-methyl-D-aspartate (NMDA).METHODS: Animals were injected intravitreally with one of six caspase inhibitors (against caspases 1, 3, 4, 6, 8 and 9). Seven hours later, NMDA or phosphate-buffered saline as a control was injected intravitreally into the respective eyes. The neuroprotective potential against NMDA toxicity was assessed by retinal ganglion cell quantification. Additionally, wholemount TUNEL was performed.RESULTS: Statistical analysis revealed significant neuroprotective effects for the inhibitors of caspases 3, 6, 8 and 9, but not for those of caspases 1 and 4. The inhibitors of caspases 6 and 9 showed greater neuroprotective potential than those of caspases 3 and 8, although cell death was not entirely averted in any case. Results of ganglion cell counts were confirmed for the most pronounced treatment groups using wholemount TUNEL.CONCLUSION: Excitotoxic retinal ganglion cell death after NMDA injection is mediated mainly through apoptosis, whereby extrinsic as well as intrinsic pathways of caspase activation play a role.

AB - BACKGROUND: Apoptosis is a major mechanism of cell death in glutamate-induced excitotoxicity and caspases as the executors of apoptosis play an important role in the development of various central nervous system and eye diseases. We studied the involvement of certain caspases in excitotoxic retinal ganglion cell death, which was experimentally induced in Brown Norway Rats by application of the glutamate receptor agonist N-methyl-D-aspartate (NMDA).METHODS: Animals were injected intravitreally with one of six caspase inhibitors (against caspases 1, 3, 4, 6, 8 and 9). Seven hours later, NMDA or phosphate-buffered saline as a control was injected intravitreally into the respective eyes. The neuroprotective potential against NMDA toxicity was assessed by retinal ganglion cell quantification. Additionally, wholemount TUNEL was performed.RESULTS: Statistical analysis revealed significant neuroprotective effects for the inhibitors of caspases 3, 6, 8 and 9, but not for those of caspases 1 and 4. The inhibitors of caspases 6 and 9 showed greater neuroprotective potential than those of caspases 3 and 8, although cell death was not entirely averted in any case. Results of ganglion cell counts were confirmed for the most pronounced treatment groups using wholemount TUNEL.CONCLUSION: Excitotoxic retinal ganglion cell death after NMDA injection is mediated mainly through apoptosis, whereby extrinsic as well as intrinsic pathways of caspase activation play a role.

KW - Animals

KW - Apoptosis/drug effects

KW - Caspase Inhibitors

KW - Cell Count

KW - Cell Survival

KW - Cytoprotection

KW - Enzyme Inhibitors/pharmacology

KW - Excitatory Amino Acid Agonists/toxicity

KW - Female

KW - In Situ Nick-End Labeling

KW - Intravitreal Injections

KW - N-Methylaspartate/toxicity

KW - Rats

KW - Rats, Inbred BN

KW - Rats, Long-Evans

KW - Retinal Ganglion Cells/drug effects

U2 - 10.1111/j.1442-9071.2010.02486.x

DO - 10.1111/j.1442-9071.2010.02486.x

M3 - SCORING: Journal article

C2 - 21176044

VL - 39

SP - 545

EP - 554

JO - CLIN EXP OPHTHALMOL

JF - CLIN EXP OPHTHALMOL

SN - 1442-6404

IS - 6

ER -