myopia/protease

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Basic fibroblast growth factor suppresses retinal neuronal apoptosis in form-deprivation myopia in chicks.

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OBJECTIVE Chorioretinal atrophy including retinal neuronal apoptosis occurred in chronic form-deprivation myopia induced by lid suture in chicks. We investigated whether exogenous basic fibroblast growth factor (bFGF) could simultaneously inhibit the excessive axial elongation and retinal neuronal

Scleral matrix metalloproteinases, serine proteinase activity and hydrational capacity are increased in myopia induced by retinal image degradation.

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In the avian model of myopia, retinal image degradation quickly leads to ocular enlargement. We now give evidence that regionally specific changes in ocular size are correlated with both biomechanical indices of scleral remodeling, e.g. hydration capacity and with biochemical changes in proteinase

Proteases in eye development and disease.

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The eye is one of the classical systems in developmental biology. Furthermore, diseases of the eye, many of which have a developmental basis, have devastating effects that often result in blindness. Proteases have diverse roles in ocular physiology and pathophysiology. Here, a broad overview is

Cause and Effect Relationship between Changes in Scleral Matrix Metallopeptidase-2 Expression and Myopia Development in Mice.

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Myopia is a serious sight-compromising condition in which decreases in scleral biomechanical strength are associated with protease up-regulation resulting in thinning of its collagenous framework and changes in the extracellular matrix composition. Matrix metallopeptidase (MMP)-2 is one of the known

Mutations in LRPAP1 are associated with severe myopia in humans.

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Myopia is an extremely common eye disorder but the pathogenesis of its isolated form, which accounts for the overwhelming majority of cases, remains poorly understood. There is strong evidence for genetic predisposition to myopia, but determining myopia genetic risk factors has been difficult to

Vitreous Proteomics Provides New Insights into Antivascular Endothelial Growth Factor Therapy for Pathologic Myopia Choroid Neovascularization.

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This study aimed to investigate the protein expression profile of vitreous humor (VH) from pathologic myopic retinoschisis (PMRS) patients with or without intravitreal antivascular endothelial growth factor (anti-VEGF) therapy. VH samples from PMRS patients were subjected to proteomic analysis.

[Intracellular pathways leading to apoptosis of retinal cells].

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Some ocular diseases, such as retinitis pigmentosa, age-related macular degeneration, glaucoma, retinal detachment, diabetic retinopathy or pathological myopia result in apoptotic death of retinal cells. Caspases are proteases that take part in the intracellular signaling pathways that cause

Peripheral melt of flap after laser in situ keratomileusis.

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BACKGROUND Laser in situ keratomileusis (LASIK) is an effective procedure to correct myopia. It may have complications related to the flap, such as epithelial ingrowth and stromal melt. METHODS We report on a patient who developed extensive epithelial ingrowth and partial keratolysis of the flap

Fold conservation and proteolysis in zebrafish IRBP structure: Clues to possible enzymatic function?

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Multiple functions for Interphotoreceptor Retinoid-Binding Protein (IRBP) may explain its localization in the retina, vitreous and pineal gland and association with retinitis pigmentosa and myopia. We have been engaged in uncovering the structure-function relationships of this interesting protein

Müller glia-derived PRSS56 is required to sustain ocular axial growth and prevent refractive error.

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A mismatch between optical power and ocular axial length results in refractive errors. Uncorrected refractive errors constitute the most common cause of vision loss and second leading cause of blindness worldwide. Although the retina is known to play a critical role in regulating ocular growth and

Extreme hyperopia is the result of null mutations in MFRP, which encodes a Frizzled-related protein.

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Nanophthalmos is a rare disorder of eye development characterized by extreme hyperopia (farsightedness), with refractive error in the range of +8.00 to +25.00 diopters. Because the cornea and lens are normal in size and shape, hyperopia occurs because insufficient growth along the visual axis places

A novel nonsense mutation in ADAMTS17 caused autosomal recessive inheritance Weill-Marchesani syndrome from a Chinese family.

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Weill-Marchesani syndrome (WMS) is a rare connective tissue disorder characterized by short stature, brachydactyly, joint stiffness, eye anomalies, including microspherophakia, ectopia of the lenses, severe myopia, glaucoma and occasionally heart defects. Given these complex clinical manifestations

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