Journal
NEUROSCIENCE LETTERS
Volume 554, Issue -, Pages 99-104Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2013.08.057
Keywords
Glaucoma; Elevated hydrostatic pressure; Mitochondrial fission; DRP1; GSK3 beta
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Funding
- International Cooperation of the National Natural Science Foundation of China [NSFC 81020108017]
- National Natural Science Foundation of China [NSFC81070726]
- Shanghai Natural Science Foundation [11ZR1405800]
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Elevated intraocular pressure (IOP) is considered as the major risk factor for the loss of retinal ganglion cells (RGCs) and their axons in glaucoma. Emerging evidence suggests elevated IOP can induce Drp1 upregulation and mitochondrial fission, which is involved in cell death. However, the underlying mechanism for these effects remains unknown. The present study used RNAi screening to investigate the effects of 24 kinases associated with mitochondrial activities on DRP1 expression under hydrostatic pressure. We identified, for the first time, that glycogen synthase kinase 3 beta (GSK3 beta) knockdown suppressed the upregulation of DRP1 induced by elevated pressure. Use of the pharmacological inhibitor of GSK3 beta inhibitor, lithium chloride (LiC1), confirmed this result. Furthermore, we demonstrated that one of the mechanisms of lithium chloride neuroprotection might be via inhibition of mitochondrial fission through downregulation of Drp1. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
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