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The role of butyrylcholinesterase in neural stem cell differentiation
Descriptive
TitleInfo
Title
The role of butyrylcholinesterase in neural stem cell differentiation
Name
(type = personal)
NamePart
(type = family)
Tiethof
NamePart
(type = given)
Angela Karin
NamePart
(type = date)
1976-
DisplayForm
Angela Karin Tiethof
Role
RoleTerm
(authority = RULIB)
author
Name
(type = personal)
NamePart
(type = family)
Hart
NamePart
(type = given)
Ronald P
DisplayForm
Ronald P Hart
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
chair
Name
(type = corporate)
NamePart
Rutgers University
Role
RoleTerm
(authority = RULIB)
degree grantor
Name
(type = corporate)
NamePart
Graduate School - New Brunswick
Role
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(authority = RULIB)
school
TypeOfResource
Text
Genre
(authority = marcgt)
theses
OriginInfo
DateCreated
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2017
DateOther
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(type = degree)
2017-01
CopyrightDate
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2017
Place
PlaceTerm
(type = code)
xx
Language
LanguageTerm
(authority = ISO639-2b);
(type = code)
eng
Abstract
(type = abstract)
Butyrylcholinesterase (BChE) is the evolutionary counterpart to acetylcholinesterase (AChE). Both enzymes appear early in nervous system development prior to cholinergic synapse formation. The organophosphate pesticide chlorpyrifos (CPS) primarily exerts toxicity through inhibition of AChE, which results in excess cholinergic stimulation at the synapse. We hypothesized that CPS inhibition of AChE and BChE may impair neurogenesis in neural stem cells (NSCs). To model neurodevelopment in vitro, we used human NSCs derived from induced pluripotent stem cells (iPSCs). After six days of differentiation, BChE activity and mRNA expression significantly increased, while AChE activity and expression remained unchanged. Utilizing CPS as a tool to inhibit the enzymatic activity of the enzymes resulted in 82% and 97% inhibition of AChE and BChE, respectively. CPS exposure had no obvious effect on cell morphology, viability or the expression of differentiation markers HES5, DCX or MAP2. However, shRNA-knockdown of BChE expression resulted in significantly decreased expression of bHLH transcription factors HES5 and HES3, and significantly increased expression of HES1 and the Notch pathway ligand Jagged 1 (JAG1). Results indicate BChE may have a role in the differentiation of NSCs independent of, or in addition to, its enzymatic activity.
Subject
(authority = RUETD)
Topic
Toxicology
Subject
(authority = ETD-LCSH)
Topic
Butyrylcholinesterase
RelatedItem
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TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier
(type = RULIB)
ETD
Identifier
ETD_7874
PhysicalDescription
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electronic resource
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
1 online resource (vii, 47 p. : ill.)
Note
(type = degree)
M.S.
Note
(type = bibliography)
Includes bibliographical references
Note
(type = statement of responsibility)
by Angela Karin Tiethof
RelatedItem
(type = host)
TitleInfo
Title
Graduate School - New Brunswick Electronic Theses and Dissertations
Identifier
(type = local)
rucore19991600001
Location
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(displayLabel = Rutgers, The State University of New Jersey)
NjNbRU
Identifier
(type = doi)
doi:10.7282/T38P62Z4
Genre
(authority = ExL-Esploro)
ETD graduate
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Rights
RightsDeclaration
(ID = rulibRdec0006)
The author owns the copyright to this work.
RightsHolder
(type = personal)
Name
FamilyName
Tiethof
GivenName
Angela
MiddleName
Karin
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime
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(qualifier = exact);
(point = start)
2017-01-13 22:20:49
AssociatedEntity
Name
Angela Tiethof
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
(ID = TECHNICAL1)
ContentModel
ETD
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windows xp
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1.5
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Microsoft® Word 2016
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2017-01-27T14:16:37
DateCreated
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2017-01-27T14:16:37
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