Investigating the role of Ca 2+/calmodulin-dependent protein kinase II in the survival of retinal ganglion cells

Xinzheng Guo; Bo Chen

doi:10.4103/1673-5374.324844

Investigating the role of Ca 2+/calmodulin-dependent protein kinase II in the survival of retinal ganglion cells

Xinzheng Guo, Bo Chen

Research output: Contribution to journal › Review article › peer-review

1 Scopus citations

Original language	English
Pages (from-to)	1001-1002
Number of pages	2
Journal	Neural Regeneration Research
Volume	17
Issue number	5
DOIs	https://doi.org/10.4103/1673-5374.324844
State	Published - May 2022

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10.4103/1673-5374.324844

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@article{a1a0ad299b3f455eb7769a336a36f6d0,

title = "Investigating the role of Ca 2+/calmodulin-dependent protein kinase II in the survival of retinal ganglion cells",

author = "Xinzheng Guo and Bo Chen",

note = "Funding Information: activity was found to be elevated for short activities change in RGCs after excitotoxicofCaMKII willhelp answerhowCaMKII periods of time andthendecreasedafter injury. Furthermore, modulation of CaMKII intravitreal injection of NMDA (Laabich activity by AAV-mediated gene delivery of and Cooper, 2000; Takeda et al., 2007). constitutively active or kinase dead mutants Interestingly, co-treatment of the CaMKII of CaMKII will help answer how CaMKII may inhibitor AIP (myristoylated autocamtide-protect RGCs from excitotoxic cell death. 2-related inhibitory peptide) with NMDA Once we know more about what CaMKII partially protected RGCs from excitotoxic cell does in RGCs after excitotoxic injury, future death (Laabich and Cooper, 2000; Goebel, studies can be expanded to examine the 2009). However, siRNA-mediated CaMKII role of CaMKII in other RGC disease/injury knockdown significantly accelerated NMDA ? models, such as optic nerve crush and induced RGC loss in another study (Takeda glaucoma models. It remains to be seen et al., 2007). These seemingly contradictory whether CaMKII can be used as a general results are reminiscent of those obtained therapeutic target for protection of RGCs and from cortical neuron cultures 唀 where CaMKII preservation of vision ? inhibition seems to be neuroprotective immediately after the excitotoxic insult, The present work was supported by National however, it induces neuronal death in a long Institutes of Health 唀 Nos 堀 R  EY  aCn 爀d Editors 圀 ?hao M 唀 ?hao LJ 唀 Qiu Y 嘀 T 爀Editor 圀 Jia Y period of time 縀Ashpole and Hudmon 唀 R 缃 E堀Y   縁? o BC 缃?",

year = "2022",

month = may,

doi = "10.4103/1673-5374.324844",

language = "English",

volume = "17",

pages = "1001--1002",

journal = "Neural Regeneration Research",

issn = "1673-5374",

publisher = "Wolters Kluwer Medknow Publications",

number = "5",

}

TY - JOUR

T1 - Investigating the role of Ca 2+/calmodulin-dependent protein kinase II in the survival of retinal ganglion cells

AU - Guo, Xinzheng

AU - Chen, Bo

N1 - Funding Information: activity was found to be elevated for short activities change in RGCs after excitotoxicofCaMKII willhelp answerhowCaMKII periods of time andthendecreasedafter injury. Furthermore, modulation of CaMKII intravitreal injection of NMDA (Laabich activity by AAV-mediated gene delivery of and Cooper, 2000; Takeda et al., 2007). constitutively active or kinase dead mutants Interestingly, co-treatment of the CaMKII of CaMKII will help answer how CaMKII may inhibitor AIP (myristoylated autocamtide-protect RGCs from excitotoxic cell death. 2-related inhibitory peptide) with NMDA Once we know more about what CaMKII partially protected RGCs from excitotoxic cell does in RGCs after excitotoxic injury, future death (Laabich and Cooper, 2000; Goebel, studies can be expanded to examine the 2009). However, siRNA-mediated CaMKII role of CaMKII in other RGC disease/injury knockdown significantly accelerated NMDA ? models, such as optic nerve crush and induced RGC loss in another study (Takeda glaucoma models. It remains to be seen et al., 2007). These seemingly contradictory whether CaMKII can be used as a general results are reminiscent of those obtained therapeutic target for protection of RGCs and from cortical neuron cultures 唀 where CaMKII preservation of vision ? inhibition seems to be neuroprotective immediately after the excitotoxic insult, The present work was supported by National however, it induces neuronal death in a long Institutes of Health 唀 Nos 堀 R  EY  aCn 爀d Editors 圀 ?hao M 唀 ?hao LJ 唀 Qiu Y 嘀 T 爀Editor 圀 Jia Y period of time 縀Ashpole and Hudmon 唀 R 缃 E堀Y   縁? o BC 缃?

PY - 2022/5

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U2 - 10.4103/1673-5374.324844

DO - 10.4103/1673-5374.324844

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AN - SCOPUS:85116411311

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JO - Neural Regeneration Research

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