Abstract
This study used isotope-coded protein label (ICPL) quantitative proteomics and bioinformatics analysis to examine changes in vitreous protein content and associated pathways during lens-induced eye growth. First, the vitreous protein profile of normal 7-day old chicks was characterized by nano-liquid chromatography electrospray ionization tandem mass spectrometry. A total of 341 unique proteins were identified. Next, myopia and hyperopia were induced in the same chick by attaching −10D lenses to the right eye and +10D lenses to the left eye, for 3 and 7 days. Protein expression in lens-induced ametropic eyes was analyzed using the ICPL approach coupled to LCMS. Four proteins (cystatin, apolipoprotein A1, ovotransferrin, and purpurin) were significantly up-regulated in the vitreous after 3 days of wearing −10D lenses relative to +10D lens contralateral eyes. The differences in protein expression were less pronounced after 7 days when the eyes approached full compensation. In a different group of chicks, western blot confirmed the up-regulation of apolipoprotein A1 and ovotransferrin in the myopic vitreous relative to both contralateral lens-free eyes and hyperopic eyes in separate animals wearing +10D lenses. Bioinformatics analysis suggested oxidative stress and lipid metabolism as pathways involved in compensated ocular elongation.
Highlights
Myopia, the most common type of refractive error, has become a global public health issue[1,2]
The vitreous fluid is protected by the blood-retinal barrier, and it has been suggested that changes in the protein composition of the vitreous occur in vitreoretinal and other ocular diseases[21,22,23]
While in a previous study we showed that retinal dopamine is the source of vitreous dopamine and dopamine levels in retina and vitreous are regulated in concordant fashion, this may not be necessarily case for apolipoprotein A1 or other proteins
Summary
The most common type of refractive error, has become a global public health issue[1,2]. Myopia has been extensively studied using environmentally-induced animal models, in various species, including monkey[9], tree shrew[10], chick[11], and guinea pig[12] They have provided good platforms to study GO (accelerating ocular growth and tune refractive status to myopia) and STOP signals (retarding ocular growth and tune refractive status to hyperopia) in regulating ocular growth and refractive error progression[13]. Advances in proteomic technology including labeling techniques, have dramatically improved large-scale identification and quantification of tissue proteomes in recent decades[27] These techniques have been applied to myopia models and several GO or STOP signals in different ocular tissues, mainly in the retina, have been identified during myopic growth[28,29,30,31]. Its expression level decreased when the eye approached the completion of emmetropization during physiological eye development[32], and in lens induced hyperopia in chick models[28]
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