The Role of Exosome Communication in Normal Ocular Function and Disease

Persistent Link:
http://hdl.handle.net/10150/579294
Title:
The Role of Exosome Communication in Normal Ocular Function and Disease
Author:
Locke, Christina Joan
Issue Date:
2015
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
Purpose: Age-related macular degeneration (AMD) and glaucoma are respectively the first and second leading causes of blindness in the United States. Mutations in the protein myocilin are known to cause glaucoma, and myocilin is only released from ocular tissues on the surface of nanovesicles known as exosomes. Exosomes function in cell-cell communication, and likely play a role in both of these disease. In this study, I investigate the release and regulation of exosomes from the retinal pigment epithelium (RPE) and the ciliary body (CB) to characterize exosome production in healthy tissues. Results: RPE and CB constitutively release large quantities of exosomes in situ, and these exosomal populations are different from one another. L-DOPA stimulation causes a drastic reduction in exosome release from both the RPE and CB, and dopamine cause a similar reduction in RPE but is variable in CB. Conclusion: The release of exosomal communication vesicles can be controlled using L-DOPA in both the RPE and CB. Regulation of exosome release is likely tied to the GPCR GPR143 and its signaling, such that during endocytosis of the receptor exosome release cannot occur. Disruptions in proper exosome release likely relate to ocular disease, and warrant further study.
Type:
text; Electronic Thesis
Degree Name:
B.S.
Degree Level:
bachelors
Degree Program:
Honors College; Biology
Degree Grantor:
University of Arizona
Advisor:
McKay, Brian

Full metadata record

DC FieldValue Language
dc.language.isoen_USen
dc.titleThe Role of Exosome Communication in Normal Ocular Function and Diseaseen_US
dc.creatorLocke, Christina Joanen
dc.contributor.authorLocke, Christina Joanen
dc.date.issued2015en
dc.publisherThe University of Arizona.en
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en
dc.description.abstractPurpose: Age-related macular degeneration (AMD) and glaucoma are respectively the first and second leading causes of blindness in the United States. Mutations in the protein myocilin are known to cause glaucoma, and myocilin is only released from ocular tissues on the surface of nanovesicles known as exosomes. Exosomes function in cell-cell communication, and likely play a role in both of these disease. In this study, I investigate the release and regulation of exosomes from the retinal pigment epithelium (RPE) and the ciliary body (CB) to characterize exosome production in healthy tissues. Results: RPE and CB constitutively release large quantities of exosomes in situ, and these exosomal populations are different from one another. L-DOPA stimulation causes a drastic reduction in exosome release from both the RPE and CB, and dopamine cause a similar reduction in RPE but is variable in CB. Conclusion: The release of exosomal communication vesicles can be controlled using L-DOPA in both the RPE and CB. Regulation of exosome release is likely tied to the GPCR GPR143 and its signaling, such that during endocytosis of the receptor exosome release cannot occur. Disruptions in proper exosome release likely relate to ocular disease, and warrant further study.en
dc.typetexten
dc.typeElectronic Thesisen
thesis.degree.nameB.S.en
thesis.degree.levelbachelorsen
thesis.degree.disciplineHonors Collegeen
thesis.degree.disciplineBiologyen
thesis.degree.grantorUniversity of Arizonaen
dc.contributor.advisorMcKay, Brianen
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