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The role of Nrg1-ErbB signaling in promoting Schwann cell myelination
Descriptive
TitleInfo
Title
The role of Nrg1-ErbB signaling in promoting Schwann cell myelination
Name
(type = personal)
NamePart
(type = family)
Syed
NamePart
(type = given)
Neeraja
NamePart
(type = date)
1974-
DisplayForm
Neeraja Syed
Role
RoleTerm
(authority = RULIB)
author
Name
(type = personal)
NamePart
(type = family)
Kim
NamePart
(type = given)
Haesun A
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Haesun A Kim
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
chair
Name
(type = personal)
NamePart
(type = family)
Jonakait
NamePart
(type = given)
Miller
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Miller Jonakait
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Friedman
NamePart
(type = given)
Wilma
DisplayForm
Wilma Friedman
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Levison
NamePart
(type = given)
Steve
DisplayForm
Steve Levison
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 - Newark
Role
RoleTerm
(authority = RULIB)
school
TypeOfResource
Text
Genre
(authority = marcgt)
theses
OriginInfo
DateCreated
(qualifier = exact)
2012
DateOther
(qualifier = exact);
(type = degree)
2012-10
CopyrightDate
(qualifier = exact)
2012
Place
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(type = code)
xx
Language
LanguageTerm
(authority = ISO639-2b);
(type = code)
eng
Abstract
(type = abstract)
Myelination is important for rapid saltatory conduction of nerve signals along the axons. Under various pathological conditions, myelin is lost and rebuilding myelin is required for functional recovery. In the PNS, myelination is regulated by axonal signals. Therefore, enhancing the promyelinating signals could be used as a therapeutic strategy to improve myelin repair by endogenous or transplanted myelinating glial cells such as Schwann cells. Recent studies identified Nrg1-type III as an important promyelinating signal that regulate Schwann cell myelination. Therefore, we hypothesized that providing an ectopic Nrg1-type III signal in a soluble form would increase the myelinating potential of Schwann cells. Since Nrg1-type III is normally expressed by axons as a membrane bound protein, in Aim 1 we first characterized the signaling function and the therapeutic potential of soluble Nrg1-type III in Schwann cells. Results from this study show that soluble Nrg1-type III elicits a promyelinating effect in-vitro: it increases myelin gene expression and enhances myelination on axons that express low levels of Nrg1-type III. However, when used at high concentrations it has a contrasting effect and inhibits myelination. Remyelination in the adult PNS is often incomplete: the myelin segments are thin and short. To determine the cell type that contributes to the defect, we characterized the myelination potentials of Schwann cells and neurons isolated from adult PNS in Aim 2. Results show that while adult Schwann cells myelinate normally, the axons provide insufficient promyelinating signals by expressing low levels of Nrg1-type III. In Aim 3, we investigated whether providing ectopic Nrg1-type III improves myelination on adult axons. Surprisingly, neither treatment with soluble nor over expressing membrane bound Nrg1-type III was sufficient to enhance myelination on adult axons. Further analysis revealed that adult axons increases Erk1/2 activity in the associated Schwann cells, an inhibitory signal for myelination. Inhibiting those signals significantly increase myelination on adult axons.
Subject
(authority = RUETD)
Topic
Biology
RelatedItem
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TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier
(type = RULIB)
ETD
Identifier
ETD_4317
PhysicalDescription
Form
(authority = gmd)
electronic resource
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
vii, 114 p. : ill.
Note
(type = degree)
Ph.D.
Note
(type = bibliography)
Includes bibliographical references
Note
(type = vita)
Includes vita
Note
(type = statement of responsibility)
by Neeraja Syed
Subject
(authority = ETD-LCSH)
Topic
Myelination
Subject
(authority = ETD-LCSH)
Topic
Neuroglia
Identifier
(type = hdl)
http://hdl.rutgers.edu/1782.1/rucore10002600001.ETD.000066588
RelatedItem
(type = host)
TitleInfo
Title
Graduate School - Newark Electronic Theses and Dissertations
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rucore10002600001
Location
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(displayLabel = Rutgers, The State University of New Jersey)
NjNbRU
Identifier
(type = doi)
doi:10.7282/T3N878MS
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
Syed
GivenName
Neeraja
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime
(encoding = w3cdtf);
(qualifier = exact);
(point = start)
2012-09-28 11:54:20
AssociatedEntity
Name
Neeraja Syed
Role
Copyright holder
Affiliation
Rutgers University. Graduate School - Newark
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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