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Editors Selection IGR 8-3
Basic research: Optic nerve dynein
Comment by Deepak Edward on:
14010 Optic nerve dynein motor protein distribution changes with intraocular pressure elevation in a rat model of glaucoma, Martin KR; Quigley HA; Valenta D et al., Experimental Eye Research, 2006; 83: 255-262
The interruption of retrograde transport of neurotrophic factors to the retinal ganglion cell body is postulated as one of the mechanisms that may lead to retinal ganglion cell apoptosis in glaucoma. Dynein and kinesin are microtubule associated proteins that play important roles in transport of neurotrophic factors within the axon. Martin et al. (672) speculate that alterations in the axonal transport proteins may lead to disruption in delivery of trophic factors to the cell body and contribute to cell death. They used a rat model of glaucoma to study alterations in dyenin. Immunohistochemistry revealed a variable increase in dynein in the anterior optic nerve and nerve fiber layer during the first week of intraocular pressure (IOP) elevationand then a decrease at later points, with some granular labeling observed in the peripheral optic nerve posterior to the sclera. Western blotting confirmed the variable but significant increase in dyenin accumulation in the optic nerve and retina. The accumulation of dyenin (a protein involved in retrograde transport) in the anterior optic nerve and retina (i.e., closer to the cell body), following injury,is a new finding. However, the reasons behind this distribution remain unclear and need to be further investigated.
Disruption in dynein transport may lead to failure in transport of important proteins trophic for retinal ganglion cells; this process might eventually lead to retinal ganglion cell apoptosis
Based on their results, the authors suggest that disruption in dynein transport may lead to failure in transport of important proteins trophic for retinal ganglion cells and that this process might eventually lead to retinal ganglion cell apoptosis. The authors acknowledge that dynein accumulation with elevated IOP is unlikely to be mainly due to mechanical obstruction and swollen axons, but they were unable to determine conclusively whether the accumulation occurred as a primary event or a consequence secondary to other axon damage. Overall, this study is interesting, showing definite IOP elevation related alterations in an important axonal transport protein. However, whether dyenin accumulation in the rat glaucoma model represents an actual blockade in retrograde transport or an alteration in retinal ganglion cell metabolism leading to failure in transport is yet to be determined.
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