Investigators using cells designated as RGC-5 should confirm the species to be of rat origin and retinal-specific marker expression before considering their use as retinal ganglion-like cells.
IOP elevation may directly damage mitochondria in the ONH axons by promoting reduction of COX, mitochondrial fission and cristae depletion, alterations of OPA1 and Dnm1 expression, and induction of OPA1 release. Thus, interventions to preserve mitochondria may be useful for protecting against ON degeneration in glaucoma.
Elevated hydrostatic pressure triggered mitochondrial fission, abnormal cristae depletion, Drp-1 translocation, and cellular ATP reduction in differentiated RGC-5 cells. Increased understanding of the molecular mechanisms that regulate the cellular response to elevated pressure including mitochondrial fission may provide new therapeutic targets for protecting RGCs from elevated hydrostatic pressure.
Our findings suggest that CoQ10 may be a promising therapeutic strategy for ameliorating glutamate excitotoxicity and oxidative stress in glaucomatous neurodegeneration.
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