Preservation of vision after CaMKII-mediated protection of retinal ganglion cells.
Animals
Axons
/ drug effects
Brain
/ pathology
Calcium-Calmodulin-Dependent Protein Kinase Type 2
/ metabolism
Cyclic AMP Response Element-Binding Protein
/ metabolism
Cytoprotection
Dependovirus
/ metabolism
Disease Models, Animal
Enzyme Activation
/ drug effects
Glaucoma
/ genetics
Mice, Inbred C57BL
Neurotoxins
/ toxicity
Optic Nerve Injuries
/ pathology
Retinal Ganglion Cells
/ pathology
Signal Transduction
Vision, Ocular
CREB
CaMKII
RGC
RGC protection
excitotoxicity
glaucoma
optic nerve crush
vision preservation
visual function
visual pathway
Journal
Cell
ISSN: 1097-4172
Titre abrégé: Cell
Pays: United States
ID NLM: 0413066
Informations de publication
Date de publication:
05 08 2021
05 08 2021
Historique:
received:
14
01
2021
revised:
22
04
2021
accepted:
24
06
2021
pubmed:
24
7
2021
medline:
6
1
2022
entrez:
23
7
2021
Statut:
ppublish
Résumé
Retinal ganglion cells (RGCs) are the sole output neurons that transmit visual information from the retina to the brain. Diverse insults and pathological states cause degeneration of RGC somas and axons leading to irreversible vision loss. A fundamental question is whether manipulation of a key regulator of RGC survival can protect RGCs from diverse insults and pathological states, and ultimately preserve vision. Here, we report that CaMKII-CREB signaling is compromised after excitotoxic injury to RGC somas or optic nerve injury to RGC axons, and reactivation of this pathway robustly protects RGCs from both injuries. CaMKII activity also promotes RGC survival in the normal retina. Further, reactivation of CaMKII protects RGCs in two glaucoma models where RGCs degenerate from elevated intraocular pressure or genetic deficiency. Last, CaMKII reactivation protects long-distance RGC axon projections in vivo and preserves visual function, from the retina to the visual cortex, and visually guided behavior.
Identifiants
pubmed: 34297923
pii: S0092-8674(21)00799-6
doi: 10.1016/j.cell.2021.06.031
pmc: PMC8530265
mid: NIHMS1721071
pii:
doi:
Substances chimiques
Cyclic AMP Response Element-Binding Protein
0
Neurotoxins
0
Calcium-Calmodulin-Dependent Protein Kinase Type 2
EC 2.7.11.17
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
4299-4314.e12Subventions
Organisme : NEI NIH HHS
ID : P30 EY026878
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH124992
Pays : United States
Organisme : NEI NIH HHS
ID : R01 EY014454
Pays : United States
Organisme : NEI NIH HHS
ID : R21 EY029806
Pays : United States
Organisme : NEI NIH HHS
ID : R01 EY028921
Pays : United States
Organisme : NEI NIH HHS
ID : R01 EY015788
Pays : United States
Organisme : NEI NIH HHS
ID : R01 EY024986
Pays : United States
Organisme : NEI NIH HHS
ID : R01 EY022645
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2021 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of interests B.C. and X.G. have filed a US patent application, 63/154,432, 63/177,230, based on the work in this paper.
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