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J. Albon, S. Farrant, J.T. Erichsen, M.E. Boulton, M. Taylor, J.E. Morgan; Microglial Activation In Experimental Glaucoma Is Related To The Pathophysiology Of Retinal Ganglion Cell Death . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1258.
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© ARVO (1962-2015); The Authors (2016-present)
To characterise the microglial response within the optic nerve head in experimental glaucoma in relation to retinal ganglion cell death.
Unilateral ocular hypertension was induced in Norwegian Brown rats (n=25), by episcleral drainage vessel sclerosis. Intraocular pressures were monitored up to 65 days. To detect microglial response, cryosections of the optic nerve head were probed with antibodies to CD45 and MHCII (microglia and peripheral cells), Ox42 (a pan–microglia marker) and Ox41 (activated microglia). Labelling was visualised by fluorescence microscopy and images were captured and analysed using Leica QFluoro software. An indication of retinal ganglion cell (RGC) death was quantified by the TUNEL assay.
Immunofluorescence labelling for each marker was quantified as the sum of (pixel intensity x pixel number) and expressed as a function of duration, accumulative IOP or fluctuations in IOP. Elevated duration of ocular hypertension appeared to increase the number of amoeboid, intensely–labelled CD45 positive cells and resulted in a time–dependent increase in cell size up to 46 days of ocular hypertension. Intensity of labelling was significantly greater in optic nerve heads that were subjected to chronic hypertension (p<0.001) and small fluctuations in IOP (p<0.05). Interestingly no significant change in labelling intensity was identified in MHCII labelling, but increasingly amoeboid looking cells were identified with duration of ocular hypertension. OX42 and Ox41 immunolabelling appeared to be significantly increased after 11 and 20 days respectively (p<0.01), as a consequence of ocular hypertension, declining after 46 days. Values were also significantly greater in cases of large fluctuations in IOP (p<0.05). Microglial activation coincided with peaks in RGC apoptosis, and declined as apoptosis decreased.
Microglia increase in number and reactivity as a function of ocular hypertension and appear to react differentially to duration and fluctuations of IOP. Microglial activation appears to be linked to the pathophysiology of retinal ganglion cell death in experimental glaucoma.
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