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The role of ephrin-A5 in lens maintenance and vitreous humor development
Descriptive
TitleInfo
Title
The role of ephrin-A5 in lens maintenance and vitreous humor development
Name
(type = personal)
NamePart
(type = family)
Son
NamePart
(type = given)
Alexander I.
NamePart
(type = date)
1983-
DisplayForm
Alexander Son
Role
RoleTerm
(authority = RULIB)
author
Name
(type = personal)
NamePart
(type = family)
Zhou
NamePart
(type = given)
Renping
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Renping Zhou
Affiliation
Advisory Committee
Role
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(authority = RULIB)
chair
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(type = family)
Dreyfus
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Cheryl
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Cheryl Dreyfus
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Advisory Committee
Role
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(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Pintar
NamePart
(type = given)
John
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John Pintar
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Matise
NamePart
(type = given)
Michael
DisplayForm
Michael Matise
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Chen
NamePart
(type = given)
Suzie
DisplayForm
Suzie Chen
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
outside member
Name
(type = corporate)
NamePart
Rutgers University
Role
RoleTerm
(authority = RULIB)
degree grantor
Name
(type = corporate)
NamePart
Graduate School - New Brunswick
Role
RoleTerm
(authority = RULIB)
school
TypeOfResource
Text
Genre
(authority = marcgt)
theses
OriginInfo
DateCreated
(qualifier = exact)
2013
DateOther
(qualifier = exact);
(type = degree)
2013-01
Place
PlaceTerm
(type = code)
xx
Language
LanguageTerm
(authority = ISO639-2b);
(type = code)
eng
Abstract
(type = abstract)
The development of the eye requires the orchestration of precise regulatory signals and events in constructing a complex structure capable of collecting visual inputs. Recent observations have identified one group of molecules, the Eph family of receptor tyrosine kinases, to be critical in the formation of and maintenance of ocular tissues. This present work focuses on the role of the Eph ligand ephrin-A5 in the development and function of the lens and vitreous humor. We have found ephrin-A5 to be a major contributor to lens development and maintenance, as mice lacking ephrin-A5 develop cataracts. Major lens abnormalities in the ephrin-A5-/- animals are observed at postnatal stages with lens opacity occurring by P21. Examination of the expression of ephrin-A5 and its putative receptor EphA2 in the lens supports a fundamental role for this receptor-ligand complex in lens development. As alterations in lens fiber cell shape were observed in the ephrin-A5-/- lens, we examined the role of ephrin-A5 and its receptor EphA2 on the control of the adherens junction. N-cadherin localization is disrupted in the ephrin-A5-/- lens; however, β-catenin, a regulator of N-cadherin interaction with the actin cytoskeleton, remains on the membrane in the ephrin-A5-/- lens and co-localizes with EphA2. Further examinations reveal Ephrin-A5 and EphA2 to regulate β-catenin interaction with N-cadherin, indicate that ephrin-A5 is required for maintaining proper lens fiber cell architecture through the regulation of the adherens junction. We have also identified critical roles of ephrin-A5 in regression of the primary vitreous. Failure of this event results in the eye disease Persistent Hyperplastic Primary Vitreous (PHPV). Ephrin-A5-/- animals develop phenotypes representative of PHPV, most notably the presence a large hyperplastic mass posterior to the lens that remains throughout the lifetime of the animal. The aberrant tissue consists of vascularized cells surrounded by pigmented cells of neural crest origin. The mass in ephrin-A5-/- animals was also found to be mitotically active in both embryonic and postnatal stages signifying that ephrin-A5 has a role in cell cycle regulation in the developing vitreous. Together, these studies demonstrate the critical and varied roles of ephrin-A5 throughout ocular development.
Subject
(authority = RUETD)
Topic
Neuroscience
RelatedItem
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TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier
(type = RULIB)
ETD
Identifier
ETD_4431
PhysicalDescription
Form
(authority = gmd)
electronic resource
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
xiii, 130 p. : ill.
Note
(type = degree)
Ph.D.
Note
(type = bibliography)
Includes bibliographical references
Note
(type = statement of responsibility)
by Alexander I. Son
Subject
(authority = ETD-LCSH)
Topic
Protein-tyrosine kinase--Receptors
Subject
(authority = ETD-LCSH)
Topic
Vitreous body--Diseases
Subject
(authority = ETD-LCSH)
Topic
Vitreous humor
Identifier
(type = hdl)
http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000067846
RelatedItem
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TitleInfo
Title
Graduate School - New Brunswick Electronic Theses and Dissertations
Identifier
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rucore19991600001
Location
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(displayLabel = Rutgers, The State University of New Jersey)
NjNbRU
Identifier
(type = doi)
doi:10.7282/T3PN94BD
Genre
(authority = ExL-Esploro)
ETD doctoral
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Rights
RightsDeclaration
(ID = rulibRdec0006)
The author owns the copyright to this work.
RightsHolder
(type = personal)
Name
FamilyName
Son
GivenName
Alexander
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime
(encoding = w3cdtf);
(qualifier = exact);
(point = start)
2012-12-18 10:13:08
AssociatedEntity
Name
Alexander Son
Role
Copyright holder
Affiliation
Rutgers University. Graduate School - New Brunswick
AssociatedObject
Type
License
Name
Author Agreement License
Detail
I hereby grant to the Rutgers University Libraries and to my school the non-exclusive right to archive, reproduce and distribute my thesis or dissertation, in whole or in part, and/or my abstract, in whole or in part, in and from an electronic format, subject to the release date subsequently stipulated in this submittal form and approved by my school. I represent and stipulate that the thesis or dissertation and its abstract are my original work, that they do not infringe or violate any rights of others, and that I make these grants as the sole owner of the rights to my thesis or dissertation and its abstract. I represent that I have obtained written permissions, when necessary, from the owner(s) of each third party copyrighted matter to be included in my thesis or dissertation and will supply copies of such upon request by my school. I acknowledge that RU ETD and my school will not distribute my thesis or dissertation or its abstract if, in their reasonable judgment, they believe all such rights have not been secured. I acknowledge that I retain ownership rights to the copyright of my work. I also retain the right to use all or part of this thesis or dissertation in future works, such as articles or books.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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Technical
RULTechMD
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ContentModel
ETD
OperatingSystem
(VERSION = 5.1)
windows xp
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