Inherited Retinal Degeneration: Towards the Development of a Combination Therapy Targeting Histone Deacetylase, Poly (ADP-Ribose) Polymerase, and Calpain

Inherited Retinal Degeneration: Towards the Development of a Combination Therapy Targeting Histone Deacetylase, Poly (ADP-Ribose) Polymerase, and Calpain

Inherited retinal degeneration (IRD) represents a diverse group of gene mutation-induced blinding diseases. In IRD, the loss of photoreceptors is often connected to excessive activation of histone-deacetylase (HDAC), poly-ADP-ribose-polymerase (PARP), and calpain-type proteases (calpain). Moreover,...

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Published in:Biomolecules (Basel, Switzerland) Vol. 13; no. 4; p. 581
Main Authors: Dong, Yujie, Yan, Jie, Yang, Ming, Xu, Wenrong, Hu, Zhulin, Paquet-Durand, François, Jiao, Kangwei
Format: Journal Article
Language:English
Published: Switzerland MDPI AG 23-03-2023
MDPI
Subjects:
Animal welfare
Animals
Apoptosis
Calpain
Calpain - metabolism
Care and treatment
Cell death
cGMP
Combination therapy
Enzymes
Genetic aspects
Health aspects
Histone deacetylase
Histone Deacetylases
Histones
Kinases
Mice
photoreceptor cell death
Photoreceptor Cells, Vertebrate
Photoreceptors
Physiological aspects
PKG
Point mutation
Poly(ADP-ribose) polymerase
Poly(ADP-ribose) Polymerase Inhibitors - pharmacology
Poly(ADP-ribose) Polymerase Inhibitors - therapeutic use
Poly(ADP-ribose) Polymerases - metabolism
Retina
Retinal degeneration
Retinal Degeneration - drug therapy
Retinal Degeneration - genetics
retinitis pigmentosa
Ribose - pharmacology
Ribose - therapeutic use
Vorinostat - pharmacology
Vorinostat - therapeutic use
China
New York
Sweden
United Kingdom > UK
United States > US
Germany
photoreceptor cell death
retinitis pigmentosa
cGMP
PKG
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Abstract Inherited retinal degeneration (IRD) represents a diverse group of gene mutation-induced blinding diseases. In IRD, the loss of photoreceptors is often connected to excessive activation of histone-deacetylase (HDAC), poly-ADP-ribose-polymerase (PARP), and calpain-type proteases (calpain). Moreover, the inhibition of either HDACs, PARPs, or calpains has previously shown promise in preventing photoreceptor cell death, although the relationship between these enzyme groups remains unclear. To explore this further, organotypic retinal explant cultures derived from wild-type mice and mice as a model for IRD were treated with different combinations of inhibitors specific for HDAC, PARP, and calpain. The outcomes were assessed using in situ activity assays for HDAC, PARP, and calpain, immunostaining for activated calpain-2, and the TUNEL assay for cell death detection. We confirmed that inhibition of either HDAC, PARP, or calpain reduced mouse photoreceptor degeneration, with the HDAC inhibitor Vorinostat (SAHA) being most effective. Calpain activity was reduced by inhibition of both HDAC and PARP whereas PARP activity was only reduced by HDAC inhibition. Unexpectedly, combined treatment with either PARP and calpain inhibitors or HDAC and calpain inhibitors did not produce synergistic rescue of photoreceptors. Together, these results indicate that in photoreceptors, HDAC, PARP, and calpain are part of the same degenerative pathway and are activated in a sequence that begins with HDAC and ends with calpain.
AbstractList Inherited retinal degeneration (IRD) represents a diverse group of gene mutation-induced blinding diseases. In IRD, the loss of photoreceptors is often connected to excessive activation of histone-deacetylase (HDAC), poly-ADP-ribose-polymerase (PARP), and calpain-type proteases (calpain). Moreover, the inhibition of either HDACs, PARPs, or calpains has previously shown promise in preventing photoreceptor cell death, although the relationship between these enzyme groups remains unclear. To explore this further, organotypic retinal explant cultures derived from wild-type mice and rd1 mice as a model for IRD were treated with different combinations of inhibitors specific for HDAC, PARP, and calpain. The outcomes were assessed using in situ activity assays for HDAC, PARP, and calpain, immunostaining for activated calpain-2, and the TUNEL assay for cell death detection. We confirmed that inhibition of either HDAC, PARP, or calpain reduced rd1 mouse photoreceptor degeneration, with the HDAC inhibitor Vorinostat (SAHA) being most effective. Calpain activity was reduced by inhibition of both HDAC and PARP whereas PARP activity was only reduced by HDAC inhibition. Unexpectedly, combined treatment with either PARP and calpain inhibitors or HDAC and calpain inhibitors did not produce synergistic rescue of photoreceptors. Together, these results indicate that in rd1 photoreceptors, HDAC, PARP, and calpain are part of the same degenerative pathway and are activated in a sequence that begins with HDAC and ends with calpain.
Inherited retinal degeneration (IRD) represents a diverse group of gene mutation-induced blinding diseases. In IRD, the loss of photoreceptors is often connected to excessive activation of histone-deacetylase (HDAC), poly-ADP-ribose-polymerase (PARP), and calpain-type proteases (calpain). Moreover, the inhibition of either HDACs, PARPs, or calpains has previously shown promise in preventing photoreceptor cell death, although the relationship between these enzyme groups remains unclear. To explore this further, organotypic retinal explant cultures derived from wild-type mice and rd1 mice as a model for IRD were treated with different combinations of inhibitors specific for HDAC, PARP, and calpain. The outcomes were assessed using in situ activity assays for HDAC, PARP, and calpain, immunostaining for activated calpain-2, and the TUNEL assay for cell death detection. We confirmed that inhibition of either HDAC, PARP, or calpain reduced rd1 mouse photoreceptor degeneration, with the HDAC inhibitor Vorinostat (SAHA) being most effective. Calpain activity was reduced by inhibition of both HDAC and PARP whereas PARP activity was only reduced by HDAC inhibition. Unexpectedly, combined treatment with either PARP and calpain inhibitors or HDAC and calpain inhibitors did not produce synergistic rescue of photoreceptors. Together, these results indicate that in rd1 photoreceptors, HDAC, PARP, and calpain are part of the same degenerative pathway and are activated in a sequence that begins with HDAC and ends with calpain.
Inherited retinal degeneration (IRD) represents a diverse group of gene mutation-induced blinding diseases. In IRD, the loss of photoreceptors is often connected to excessive activation of histone-deacetylase (HDAC), poly-ADP-ribose-polymerase (PARP), and calpain-type proteases (calpain). Moreover, the inhibition of either HDACs, PARPs, or calpains has previously shown promise in preventing photoreceptor cell death, although the relationship between these enzyme groups remains unclear. To explore this further, organotypic retinal explant cultures derived from wild-type mice and mice as a model for IRD were treated with different combinations of inhibitors specific for HDAC, PARP, and calpain. The outcomes were assessed using in situ activity assays for HDAC, PARP, and calpain, immunostaining for activated calpain-2, and the TUNEL assay for cell death detection. We confirmed that inhibition of either HDAC, PARP, or calpain reduced mouse photoreceptor degeneration, with the HDAC inhibitor Vorinostat (SAHA) being most effective. Calpain activity was reduced by inhibition of both HDAC and PARP whereas PARP activity was only reduced by HDAC inhibition. Unexpectedly, combined treatment with either PARP and calpain inhibitors or HDAC and calpain inhibitors did not produce synergistic rescue of photoreceptors. Together, these results indicate that in photoreceptors, HDAC, PARP, and calpain are part of the same degenerative pathway and are activated in a sequence that begins with HDAC and ends with calpain.
Audience Academic
Author Dong, Yujie
Hu, Zhulin
Jiao, Kangwei
Xu, Wenrong
Yan, Jie
Paquet-Durand, François
Yang, Ming
AuthorAffiliation 1 Key Laboratory of Yunnan Province, Yunnan Eye Institute, Affiliated Hospital of Yunnan University, Yunnan University, 176 Qingnian, Kunming 650021, China
4 Graduate Training Centre of Neuroscience, University of Tübingen, 72076 Tübingen, Germany
3 Institute for Ophthalmic Research, University of Tübingen, 72076 Tübingen, Germany
2 Kunming Medical University, No. 1168 Chunrongxi Road, Chenggong District, Kunming 650500, China
5 Department of Ophthalmology, First Affiliated Hospital of Kunming Medical University, Kunming 650032, China
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Keywords photoreceptor cell death
retinitis pigmentosa
cGMP
PKG
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SSID ssj0000800823
Score 2.308288
Snippet Inherited retinal degeneration (IRD) represents a diverse group of gene mutation-induced blinding diseases. In IRD, the loss of photoreceptors is often...
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pubmedcentral
proquest
gale
crossref
pubmed
SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
StartPage 581
SubjectTerms Animal welfare
Animals
Apoptosis
Calpain
Calpain - metabolism
Care and treatment
Cell death
cGMP
Combination therapy
Enzymes
Genetic aspects
Health aspects
Histone deacetylase
Histone Deacetylases
Histones
Kinases
Mice
photoreceptor cell death
Photoreceptor Cells, Vertebrate
Photoreceptors
Physiological aspects
PKG
Point mutation
Poly(ADP-ribose) polymerase
Poly(ADP-ribose) Polymerase Inhibitors - pharmacology
Poly(ADP-ribose) Polymerase Inhibitors - therapeutic use
Poly(ADP-ribose) Polymerases - metabolism
Retina
Retinal degeneration
Retinal Degeneration - drug therapy
Retinal Degeneration - genetics
retinitis pigmentosa
Ribose - pharmacology
Ribose - therapeutic use
Vorinostat - pharmacology
Vorinostat - therapeutic use
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Title Inherited Retinal Degeneration: Towards the Development of a Combination Therapy Targeting Histone Deacetylase, Poly (ADP-Ribose) Polymerase, and Calpain
URI https://www.ncbi.nlm.nih.gov/pubmed/37189329
https://www.proquest.com/docview/2806499479
https://search.proquest.com/docview/2814526920
https://pubmed.ncbi.nlm.nih.gov/PMC10136301
https://doaj.org/article/977321f387724f19a4062361dc580977
Volume 13
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