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Interleukin-1 mediated cell-type specific signaling in hippocampal neurons and astrocytes
Descriptive
TypeOfResource
Text
TitleInfo
(ID = T-1)
Title
Interleukin-1 mediated cell-type specific signaling in hippocampal neurons and astrocytes
Identifier
ETD_2677
Identifier
(type = hdl)
http://hdl.rutgers.edu/1782.2/rucore10002600001.ETD.000052961
Language
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(type = code)
English
Genre
(authority = marcgt)
theses
Subject
(ID = SBJ-1);
(authority = RUETD)
Topic
Biology
Subject
(ID = SBJ-2);
(authority = ETD-LCSH)
Topic
Interleukin-1
Subject
(ID = SBJ-3);
(authority = ETD-LCSH)
Topic
Neurons--Physiology
Subject
(ID = SBJ-4);
(authority = ETD-LCSH)
Topic
Astrocytes
Abstract
Interleukin-1β (IL-1β) is a pro-inflammatory cytokine that is implicated in immune and inflammatory responses. In the central nervous system (CNS), IL-1β is synthesized and released during injury, infection, and many neurodegenerative diseases, but also under physiological conditions. Several IL-1-mediated signaling pathways and effects have been identified in hippocampal neurons and astrocytes, but their mechanisms have not been fully defined. IL-1 signaling requires the type one IL-1 receptor (IL-1RI) as well as IL-1 receptor accessory protein (IL-1RAcP) as a receptor partner. A novel isoform of the IL-1 receptor accessory protein, AcPb, has also been found in the CNS, but its role remains unclear. This thesis examined AcPb function in regulating IL-1β signaling. The results showed that IL-1β activated p38 MAPK but not NFκB in neurons. In astrocytes, IL-1β induced both p38 and NFκB pathways in regulating inflammatory responses. AcPb was not involved in mediating either p38 or NFκB in either cell type. In contrast, a physiological level of IL-1β treatment (0.01ng/ml) activated p-Src in neurons via AcPb in vitro. In addition, overexpression of AcPb in astrocytes was sufficient to induce p-Src mediated by IL-1β. Taken together, these results suggest that the restricted expression of AcPb in CNS neurons may mediate neuronal specific IL-1 pathways and outcomes, and that physiological and pathophysiological levels of IL-1β mediate particular neuronal functions via separate pathways.
PhysicalDescription
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electronic resource
Extent
v, 97 p. : ill.
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application/pdf
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text/xml
Note
(type = degree)
Ph.D.
Note
Includes abstract
Note
(type = bibliography)
Includes bibliographical references
Note
(type = statement of responsibility)
by Yangyang Huang
Name
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Huang
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Yangyang
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1978-
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author
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Yangyang Huang
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(type = family)
Friedman
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(type = given)
Wilma j
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(authority = RULIB)
chair
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Advisory Committee
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Wilma j Friedman
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(type = personal)
NamePart
(type = family)
Kim
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(type = given)
Haesun
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(authority = RULIB)
internal member
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Advisory Committee
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Haesun Kim
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(ID = NAME-4);
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(type = family)
Jonakait
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(type = given)
Mill
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internal member
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Advisory Committee
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Mill Jonakait
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(ID = NAME-5);
(type = personal)
NamePart
(type = family)
Jonakait
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(type = given)
G Miller
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internal member
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Advisory Committee
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G Miller Jonakait
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(ID = NAME-6);
(type = personal)
NamePart
(type = family)
Levison
NamePart
(type = given)
Steve W
Role
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(authority = RULIB)
outside member
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Advisory Committee
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Steve W Levison
Name
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NamePart
Rutgers University
Role
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(authority = RULIB)
degree grantor
Name
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NamePart
Graduate School - Newark
Role
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(authority = RULIB)
school
OriginInfo
DateCreated
(qualifier = exact)
2010
DateOther
(qualifier = exact);
(type = degree)
2010-05
Place
PlaceTerm
(type = code)
xx
RelatedItem
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TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier
(type = RULIB)
ETD
RelatedItem
(type = host)
TitleInfo
Title
Graduate School - Newark Electronic Theses and Dissertations
Identifier
(type = local)
rucore10002600001
Location
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NjNbRU
Identifier
(type = doi)
doi:10.7282/T34X57W3
Genre
(authority = ExL-Esploro)
ETD doctoral
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Rights
RightsDeclaration
(AUTHORITY = GS);
(ID = rulibRdec0006)
The author owns the copyright to this work.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
RightsHolder
(ID = PRH-1);
(type = personal)
Name
FamilyName
Huang
GivenName
Yangyang
Role
Copyright Holder
RightsEvent
(ID = RE-1);
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Type
Permission or license
DateTime
2010-04-30 00:17:36
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Copyright holder
Name
Yangyang Huang
Affiliation
Rutgers University. Graduate School - Newark
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(AUTHORITY = rulib)
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License
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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
(ID = RE-2);
(AUTHORITY = rulib)
Type
Embargo
DateTime
2010-05-31
Detail
Access to this PDF has been restricted at the author's request. It will be publicly available after November 30th, 2010.
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Technical
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ETD
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application/pdf
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application/x-tar
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4884480
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