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Editors Selection IGR 18-4

Intraocular Pressure: Effect IOP on cytoskeletal protein F-actin

Comment by Brad Fortune on:

23913 Altered F-actin distribution in retinal nerve fiber layer of a rat model of glaucoma, Huang XR; Knighton RW, Experimental Eye Research, 2009; 88: 1107-1114

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Following their pioneering work on cytoskeletal contributions to retinal nerve fiber layer (RNFL) retardance, a measurement now utilized throughout the world for clinical glaucoma care, Huang and Knighton (604) have recently evaluated the effects of chronic intraocular pressure (IOP) elevation in an experimental model of glaucoma on the distribution of the cytoskeletal protein F-actin.¹ In this study, Wistar rats received unilateral translimbal laser photocoagulation treatments to the trabecular meshwork resulting in generally sustained IOP elevation of about 4-8 mmHg over untreated, fellow control eyes. After a period of 2-11 weeks of IOP elevation, retinas were harvested, stained with fluorescently labeled phalloidin and imaged by confocal microscopy. Phalloidin binds F-actin, a protein found throughout the retina, but which is especially strongly expressed within the RNFL. Confocal microscopy enables cross-sectional evaluation through the depth of stained retinal samples, in addition to an 'en face' view. Their results demonstrated that, in contrast to the regular, uniform distribution of F-actin within normal rat RNFL bundles, the F-actin distribution in rat eyes with experimental glaucoma was altered along and across RNFL bundles. The investigators also noted a tendency for alterations to be greatest nearer to the position of the optic nerve head (compared with more peripheral retinal locations) and greatest in dorsal retinal regions (compared to the relatively spared ventral retinal quadrant). The authors suggest that their data provide further evidence of axonal cytoskeletal abnormalities preceding total structural loss of retinal ganglion cell axons from the RNFL. However, this study was unable to distinguish unequivocally between those two possibilities, having used and analyzed only the phalloidin stain. That is, retrograde degeneration from the optic nerve toward ganglion cell bodies ‐ if imaged during the appropriate stage ‐ could produce the observed staining pattern, in particular, the relative preservation of peripheral phalloidin staining. Nevertheless, the results of this paper are interesting and provide further evidence of non-uniform susceptibility across the retina of retinal ganglion cells (and their axons) to chronic IOP elevation.

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