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      Proteomic analysis of aqueous humor from patients with myopia

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          Abstract

          Purpose

          The mechanism of axial elongation in the myopic eyeball remains to be elucidated. It is known that the expression profile for some proteins in the aqueous humor (AH) changes in some diseases. Accordingly, determinations of these AH proteins may serve to understand their potential role in this pathogenesis. To identify the possible mechanism in myopia development, a proteomic analysis of the AH composition from high myopic eyes (patients) was performed and compared with that of the AH composition from non-myopic cataract eyes (controls).

          Methods

          Total protein concentration in AH was determined by the Bradford method, and separation profiles were analyzed by two-dimensional (2D) gel electrophoresis. Protein in gel was determined by silver stain, and the separation profiles were analyzed to assess spot density changes between myopia and non-myopia patients. These spots in gel were isolated and identified by mass spectrometry.

          Results

          The total protein concentration in AH with high myopia was significantly greater than that of non-myopia. A total of six spots were significantly increased in 2D gels from high myopia. The spots were derived from albumin, transthyretin, and a vitamin D-binding protein.

          Conclusions

          The protein composition in AH was significantly different between myopia and non-myopia. The identified proteins could be a potential biomarker for high myopia development and may play a role in the mechanisms of myopia ocular axial elongation.

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          Most cited references 34

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          Choroidal and scleral mechanisms of compensation for spectacle lenses in chicks.

          It is known that when hyperopic or myopic defocus is imposed on chick eyes by spectacle lenses, they rapidly compensate, becoming myopic or hyperopic respectively, by altering the depth of their vitreous chamber. Changes in two components--ocular length and choroidal thickness--underlie this rapid compensation. With monocular lens treatment, hyperopic defocus imposed by negative lenses resulted in substantially increased ocular elongation and a slight thinning of the choroid, both changes resulting in myopia; myopic defocus imposed by positive lenses resulted a dramatic increase in choroidal thickness, which pushed the retina forward toward the image plane, and a slight decrease in ocular elongation, both changes resulting in hyperopia. The refractive error after 5 days of lens wear correlated well with vitreous chamber depth, which reflected the changes in both choroidal thickness and ocular length. The degree of compensation for lenses was not affected by whether the fellow eye was covered or open. Both form-deprivation myopia and lens-induced myopia declined with age in parallel, but wearing a -15 D lens produced more myopia than did form deprivation. The spectacle lenses affected the refractive error not only of the lens-wearing eye, but also, to a much lesser degree, of the untreated fellow eye. At lens removal refractive errors were opposite in sign to the lense worn, and the subsequent changes in choroidal thickness and ocular length were also opposite to those that occurred when the lenses were in place. In this situation as well, effects of the spectacle lenses on the fellow eyes were observed. Eyes with no functional afferent connection to the brain because of either prior optic nerve section or intraocular tetrodotoxin injections showed compensatory changes to imposed defocus, but these were limited to compensation for imposed myopic defocus, at least for the eyes with optic nerve section. In addition, optic nerve section, but not tetrodotoxin treatment, moved the set-point of the visual compensatory mechanism toward hyperopia. Optic nerve section prevents myopia in response to negative lenses but not to diffusers, suggesting that compensation for hyperopia requires the central nervous system.
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            Aqueous humor levels of vascular endothelial growth factor and pigment epithelium-derived factor in polypoidal choroidal vasculopathy and choroidal neovascularization.

            To determine the aqueous levels of vascular endothelial growth factor (VEGF) and pigment epithelium-derived factor (PEDF) in patients with active polypoidal choroidal vasculopathy (PCV) and choroidal neovascularization (CNV) secondary to age-related macular degeneration (AMD) and pathologic myopia. Prospective, comparative control study. Aqueous humors were collected from 32 eyes of 32 patients for either active PCV or CNV. Among them, 11 eyes had active and symptomatic PCV, 12 eyes had active CNV secondary to AMD, and nine eyes had active CNV of pathologic myopia. Levels of VEGF and PEDF were determined by commercially available enzyme-linked immunosorbent assay kits. A group of 10 aqueous samples from 10 patients who underwent cataract surgery without other ocular or systemic diseases comprised the controls. VEGF concentrations in aqueous humor were markedly increased in patients with PCV, CNV of AMD, and CNV of myopia when compared with the controls (analysis of variance [ANOVA], P < .001). VEGF levels in eyes with PCV were, however, significantly lower than those of exudative AMD (P = .045). The PEDF levels were also significantly different among the groups (ANOVA, P = .001), and we observed increased levels in PCV, CNV of AMD, and CNV of myopia. VEGF and PEDF factors were coexpressed and increased with positive correlation in aqueous humor of eyes with active PCV. The different levels of both factors in eyes of PCV and AMD might suggest distinct clinical entities or different angiogenesis courses between PCV and AMD.
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              TGFbeta2-induced changes in human trabecular meshwork: implications for intraocular pressure.

              Transforming growth factor (TGF)-beta2 levels are elevated in glaucomatous human aqueous humor. TGFbeta is a cytokine that alters extracellular matrix (ECM) metabolism, and excess ECM has been proposed to increase aqueous outflow resistance in the trabecular meshwork (TM) of glaucomatous eyes. This study was undertaken to investigate effects of TGFbeta2 on secretion of fibronectin and the protease inhibitor plasminogen activator inhibitor (PAI)-1 from human TM cell cultures and perfused human ocular anterior segments. Total RNA was isolated from pooled human TM cell monolayers and used for a gene microarray expression analysis. Supernatants from treated human TM cells were analyzed by ELISA for fibronectin or PAI-1 content. TGFbeta2 effects on intraocular pressure (IOP) were evaluated in a perfused organ culture model using human anterior segments, and eluates were analyzed for fibronectin and PAI-1 content. Overnight treatment of TM cells with TGFbeta2 upregulated multiple ECM-related genes, such as PAI-1. TGFbeta2 also increased secretion of both fibronectin and PAI-1 from TM cells. TGFbeta2 effects on TM cells were blocked by inhibitors of the TGFbeta type I receptor. In perfused human anterior segments, TGFbeta2 treatment elevated IOP and increased eluate fibronectin and PAI-1 content. TGFbeta2 effects on IOP may be transduced by TGFbeta type-I receptor-mediated changes in TM secretion of ECM-related factors such as fibronectin and PAI-1. Modulation of TGFbeta2-induced changes in the ECM may provide a novel and viable approach to the management of glaucoma.
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                Author and article information

                Journal
                Mol Vis
                MV
                Molecular Vision
                Molecular Vision
                1090-0535
                2008
                03 March 2008
                : 14
                : 370-377
                Affiliations
                [1 ]Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University
                [2 ]Beijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University
                [3 ]Protein Research Platform, Chinese Academy of Science, Beijing, China
                Author notes

                Dr. Duan, Dr. Lu, Professor Yang, and Professor Wang contributed equally to this publication

                Correspondence to: Ningli Wang, Department of Opthalmology, Beijing Tongren Hospital Affiliated to Capital University of Medical Science, 1 Dongjiaominxiang Street, Dongcheng District, Eye Center of Beijing Tong-Ren Hospital, Capital Medical University, Beijing, China; Phone: 8610-58269920; FAX: 8610-58269920; email: wningli@ 123456trhos.com
                Article
                45 2007MOLVIS0266
                2268849
                18334949

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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