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S. Sandmann, K. Bruns, M. Kuepper, N. Pfeiffer, F. Grus; Two–Dimensional Electrophoresis of Aqueous Humour in Glaucoma Patients: Does Transthyretin Play a Role in the Pathogenesis of Glaucoma? . Invest. Ophthalmol. Vis. Sci. 2006;47(13):202.
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Glaucoma is one of the leading causes for blindness in the world. It is usually characterized by an elevated intraocular pressure, that is thought to be a major factor for the progressive loss of retinal ganglion cells seen in glaucoma patients. To identify further mechanisms that may cause glaucomatous damage in the eye, we performed two–dimensional electrophoretical analyses of aqueous humour from glaucoma patients.
Aqueous humour samples of 52 patients with glaucoma and a control group (n=31) were collected. Patients were categorized in four main groups, i.e. primary–open–angle–glaucoma (POAG), normal–tension–glaucoma (NTG), pseudoexfoliation–glaucoma (PEX) and angle–closure–glaucoma (ACG). The protein composition of aqueous humour was analysed by using two–dimensional (2D) gel electrophoresis. Subsequently, "ImageMaster 2D Platinum Software" was used to detect protein spots in 2D gels that were differentially expressed in either the glaucoma or in the control group. Spots exhibiting clear differential abundance were identified by mass spectrometry (Lc–MSMS).
In all groups a complex pattern of protein spots could be detected. The samples of all glaucoma patients revealed some regions that were clearly different from those in controls. Particularly in POAG and PEX patients several spots were significantly increased. One of the proteins, highly abundant in the aqueous humour of glaucoma patients, was identified as transthyretin (TTR), a protein associated with the formation of insoluble protein aggregates (amyloid deposits).
Aqueous humour of glaucoma patients differs significantly in its protein composition from those of healthy eyes. Detection of elevated TTR concentration in glaucoma samples is an interesting observation. TTR may play an important role in the onset of glaucoma since it has been shown to form amyloid deposits. These particles could cause outflow obstructions, thereby increasing intraocular pressure as a possible mechanism of glaucoma onset.
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