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

          Christine Wildsoet, Josh Wallman (1995)
          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.

            Limin Liu, Yinglei Lai, Chi Pui Pang … (2006)
            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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              Structural and ultrastructural changes to the sclera in a mammalian model of high myopia.

              N McBrien, L Cornell, A Gentle (2001)
              The development of high myopia is associated with scleral thinning and changes in the diameter of scleral collagen fibrils in humans. In the present study, the association between these scleral changes and the losses in scleral tissue that have previously been reported in animal models were investigated to determine the relationship between changes in collagen fibril architecture and thinning of the sclera in high myopia. Myopia was induced in young tree shrews by monocular deprivation of pattern vision for short-term (12 days) or long-term (3-20 months) periods. Scleral tissue from normal animals over a wide age range (birth to 21 months) was also collected to provide data on the normal development of the sclera. Light and electron microscopy were used to measure scleral thickness and to determine the frequency distribution of collagen fibril diameters in the sclera. Tissue loss was monitored through measures of scleral dry weight. Significant scleral thinning and tissue loss, particularly at the posterior pole of the eye, were associated with ocular enlargement and myopia development after both short- and long-term treatments. However, collagen fibril diameter distribution was not significantly altered after short-term myopia treatment, whereas, from 3 months of monocular deprivation onward, significant reductions in the median collagen fibril diameter were noted, particularly at the posterior pole. The results of this study demonstrated that loss of scleral tissue and subsequent scleral thinning occurred rapidly during development of axial myopia. However, this initial tissue loss progressed in a way that did not result in significant alterations to the collagen fibril diameter distribution. In the longer term, there was an increased number of small diameter collagen fibrils in the sclera of highly myopic eyes, which is consistent with findings in humans and is likely to contribute to the weakened biomechanical properties of the sclera that have previously been reported.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mol Vis
                Journal ID (publisher-id): MV
                Title: Molecular Vision
                Publisher: Molecular Vision
                ISSN (Electronic): 1090-0535
                Publication date Collection: 2008
                Publication date (Electronic): 03 March 2008
                Volume: 14
                Pages: 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
                Publisher ID: 45 Publisher ID: 2007MOLVIS0266
                PMC ID: 2268849
                PubMed ID: 18334949
                SO-VID: 71752af0-9e07-4e3b-81e3-17160518391a
                Copyright statement: Copyright @ 2008
                License:

                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.

                History
                Date received : 21 August 2007
                Date accepted : 07 February 2008
                Categories
                Subject: Research Article
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                ScienceOpen disciplines: Vision sciences
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                ScienceOpen disciplines: Vision sciences

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