in vitro effects of insulin and vegf on the choroidal and scleral components of eye growth
Item
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Title
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in vitro effects of insulin and vegf on the choroidal and scleral components of eye growth
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Identifier
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d_2009_2013:7c5399b0a900:12033
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identifier
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12689
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Creator
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Sheng, Ka Lee Caren,
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Contributor
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Josh Wallman | Jonathan Levitt
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Date
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2013
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Language
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English
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Publisher
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City University of New York.
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Subject
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Biology | Neurosciences | Choroid | eye growth | Insulin | Myopia | RPE | VEGF
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Abstract
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Emmetropization occurs in most vertebrates to regulate the axial length of the growing eyes, so that the focal plane of the eye can match its ocular length, and a clear image of a distant object can fall on the retina. It has been well established that vision can control eye growth (change in the ocular length). When the image of the distant object is not on the retina, change in eye growth occurs to correct this visual error, so that the position of the retina can be moved and the image of a distant object can fall on the retina again. Visual error can be induced by using optical lenses, or by depriving the eye of form vision (form deprivation), or by allowing the eye to recover from form deprivation. The eye will compensate the induced error by changing the choroidal thickness and rate of ocular elongation. This compensation can occur without any connection to the brain, which suggests that eye growth can be regulated by local retinal signals. A signal cascade is presumed to be present at the posterior part of the eye, where retina produces the signal to act on the retinal pigment epithelium (RPE), and RPE produces another signal to affect choroid and/or sclera. It is also possible that the signal that regulates the choroid is different from the signal that regulates the sclera. Many molecules have been suggested to be involved in eye growth. Among them, insulin and vascular endothelial growth factor (VEGF) are potential regulatory signals. Insulin injected into the eye can decrease choroidal thickening caused by positive lenses and increase ocular elongation as well as scleral glycosaminoglycan (GAG) synthesis, an indicator of ocular elongation in vitro. VEGF mRNA expression in the RPE increases when eye growth is enhanced. In this thesis, we used a new experimental system to study the in vitro effect of insulin and VEGF on the choroidal and scleral components of eye growth. Eye-cups with vitreous and retina removed were prepared. The RPE and choroid of the eye-cups can be removed separately. Therefore, the effect of how the RPE and choroid mediate the effect of insulin and VEGF to affect the choroidal and scleral components (indicated by scleral GAG synthesis in vitro) of eye growth can be studied. We found that in in vitro as in in vivo, insulin can reduce choroidal thickening and increase scleral GAG synthesis. Our findings also suggest that insulin can cause the RPE to produce secondary signaling molecules that thin the choroid. Furthermore, we found that VEGF can reduce choroidal thickening transiently and increase scleral GAG synthesis in the eye-cups with choroid and sclera. We suggest that both insulin and VEGF act on the choroid to affect scleral GAG synthesis. We also suggest that insulin might cause the RPE to produce VEGF to thin the choroid, and VEGF might be one of the initial signals that cause choroidal thinning in eye growth. We suggest future experiments to explore further this relationship between insulin and VEGF in guiding eye growth.
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Type
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dissertation
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Source
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2009_2013.csv
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degree
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Ph.D.
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Program
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Biology
