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Editors Selection IGR 18-4
Basic Science: A Mouse Model for assessing ONH Damage
Comment by Richard Libby on:
72863 A mouse ocular explant model that enables the study of living optic nerve head events after acute and chronic intraocular pressure elevation: Focusing on retinal ganglion cell axons and mitochondria, Kimball EC; Pease ME; Steinhart MR et al., Experimental Eye Research, 2017; 160: 106-115
The optic nerve head (ONH) is a critical site of injury to retinal ganglion cell axons in glaucoma. The ONH consists of multiple cell types, including astrocytes and microglia, and retinal ganglion cell axons. After a glaucomatous injury, it is important to understand dynamic intracellular events in the ONH and how the different cell types interact over time. To date, it has been very difficult to study the in vivo biology of the ONH, limiting our ability to understand critical pathophysiological changes that occur with time. To overcome this limitation, Kimball and colleagues developed a mouse organ culture system specifically designed to interrogate the ONH and retinal ganglion cell axons in situ. In this manuscript, using mouse genetic tools, they ask important questions about mitochondrial biology that are relevant to glaucoma. To do this they compare mitochondrial dynamics in retinal ganglion cell axons in and around the ONH between normotensive eyes and eyes subjected to elevated intraocular pressure. They found that mitochondrial size, movement and density were all significantly different in the ocular hypertensive eyes compared to the control eyes. These data further implicate mitochondrial biology in glaucomatous neurodegeneration. A very significant aspect of this manuscript is the development of a much-needed model system that can provide critical feedback concerning cellular responses in the ONH in real time in a tractable, animal model of glaucoma. Going forward this model system could be used to ask additional important questions about ONH and retinal ganglion cell axon biology after glaucoma-relevant injuries. For example, the system could be used in conjunction with pharmaceutical or genetic manipulations to critically test hypotheses about glaucomatous neurodegeneration. Furthermore, it could be used to elucidate the precise timing of events relevant to axonal injury in microdomains of the ONH. I am looking forward to future studies from this group and others that exploit this technology to probe key aspects of glaucomatous pathophysiology.
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