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Role of notch signaling after traumatic brain injury in a transgenic mouse model

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Title
Role of notch signaling after traumatic brain injury in a transgenic mouse model
Name (type = personal)
NamePart (type = family)
Anderson
NamePart (type = given)
Jeremy
NamePart (type = date)
1993-
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Jeremy Anderson
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RoleTerm (authority = RULIB)
author
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Cai
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Li
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Li Cai
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Advisory Committee
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chair
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Firestein
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Bonnie
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Bonnie Firestein
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Advisory Committee
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internal member
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Pang
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Zhiping
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Zhiping Pang
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Advisory Committee
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RoleTerm (authority = RULIB)
internal member
Name (type = personal)
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Alder
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Janet
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Janet Alder
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Advisory Committee
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outside member
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Rutgers University
Role
RoleTerm (authority = RULIB)
degree grantor
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NamePart
School of Graduate Studies
Role
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school
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Text
Genre (authority = marcgt)
theses
OriginInfo
DateCreated (encoding = w3cdtf); (qualifier = exact)
2019
DateOther (encoding = w3cdtf); (qualifier = exact); (type = degree)
2019-10
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2019
Language
LanguageTerm (authority = ISO 639-3:2007); (type = text)
English
Abstract (type = abstract)
Traumatic brain injury (TBI) is a leading cause of disability and death in the United States and worldwide. Endogenous neural stem/progenitor cells (NSPCs) in the adult are a potential source for injury recovery. However, much about the response of injury-activated NSPCs is still unknown. Notch signaling is critical for maintaining NSPC status during embryonic development and transiently activated after injury. In the first part of this thesis, the role of Notch signaling after TBI is investigated using a Notch1CR2-GFP transgenic mouse model. During development, GFP mainly marks interneuron progenitor cells. A closed head injury (CHI) in this transgenic mouse was performed to determine the response of injury-activated NSPCs. CHI induces neuroinflammation, cell death, and the expression of typical TBI markers, validating the animal model. In addition, CHI induces cell proliferation in GFP+ cells expressing NSPC markers, e.g., Notch1 and Nestin. A significant higher percentage of GFP+ GABAergic interneurons was observed in the CHI brain, with no significant change in oligodendrocyte lineage between the CHI and sham animal groups. Since injury is known to activate astrogliosis, these results suggest that injury-induced GFP+ NSPCs preferentially differentiate into GABAergic neurons. Our study establishes that Notch1CR2-GFP transgenic mouse is a useful tool for the study of NSPC behavior in vivo after TBI.
In the second part of this thesis, the role of Gsx1, a neurogenic transcription factor, on promoting Notch1 expression and neurogenesis is investigated. A lentivirus system is used to deliver Gsx1 at the injury site after closed head injury (CHI) in the Notch1CR2-GFP transgenic mice. We identify that CHI increases GFP+ cell, during the acute phase of TBI and increasingly label neurons during the chronic phase of TBI. Lentivirus-mediated Gsx1 overexpression increases Notch1 expressing cells in the cerebral cortex and hippocampus; these virally transduced cells proliferate and mark NSPCs during the subacute phase of TBI and primarily label glutamatergic neurons during the chronic phase of TBI. The role of Gsx1 promoting Notch signaling and neurogenesis after TBI represents a new therapeutic for the treatment of TBI. Unveiling the potential of NSPCs to TBI (e.g., proliferation and differentiation) will identify new therapeutic strategy for the treatment of brain trauma.
Subject (authority = RUETD)
Topic
Biomedical Engineering
Subject (authority = LCSH)
Topic
Neural stem cells
Subject (authority = LCSH)
Topic
Transgenic mice
RelatedItem (type = host)
TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
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ETD
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ETD_10185
PhysicalDescription
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application/pdf
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text/xml
Extent
1 online resource (xiii, 100 pages) : illustrations
Note (type = degree)
Ph.D.
Note (type = bibliography)
Includes bibliographical references
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School of Graduate Studies Electronic Theses and Dissertations
Identifier (type = local)
rucore10001600001
Location
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NjNbRU
Identifier (type = doi)
doi:10.7282/t3-695z-w777
Genre (authority = ExL-Esploro)
ETD doctoral
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Rights

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The author owns the copyright to this work.
RightsHolder (type = personal)
Name
FamilyName
Anderson
GivenName
Jeremy
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2019-08-26 16:25:03
AssociatedEntity
Name
Jeremy Anderson
Role
Copyright holder
Affiliation
Rutgers University. School of Graduate Studies
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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.
RightsEvent
Type
Embargo
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2019-10-31
DateTime (encoding = w3cdtf); (qualifier = exact); (point = end)
2021-10-30
Detail
Access to this PDF has been restricted at the author's request. It will be publicly available after October 30th, 2021.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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2019-08-26T16:15:30
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