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Osteopontin as a regulator of leukemia inhibitory factor mRNA levels in the AtT-20 mouse pituitary cell line
Descriptive
TypeOfResource
Text
TitleInfo
(ID = T-1)
Title
Osteopontin as a regulator of leukemia inhibitory factor mRNA levels in the AtT-20 mouse pituitary cell line
Identifier
ETD_3150
Identifier
(type = hdl)
http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000057538
Language
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(authority = ISO639-2);
(type = code)
eng
Genre
(authority = marcgt)
theses
Subject
(ID = SBJ-1);
(authority = RUETD)
Topic
Microbiology and Molecular Genetics
Subject
(ID = SBJ-2);
(authority = ETD-LCSH)
Topic
Leukemia--Animal models
Subject
(ID = SBJ-3);
(authority = ETD-LCSH)
Topic
Leukemia--Treatment
Subject
(ID = SBJ-4);
(authority = ETD-LCSH)
Topic
Osteopontin
Abstract
(type = abstract)
The highly phosphorylated glycoprotein Osteopontin (OPN) is a multifaceted protein with a diversity of roles in many immunological processes, and has recently been found to have a significant role in the Hypothalamus-Pituitary-Adrenal (HPA) axis. Its role was discovered when unstressed OPN-knockout mice were found to have abnormally high basal corticosterone levels, which is the hormone typically elevated following stress induction of the HPA axis. Another protein rigorously studied and repeatedly identified in the successful functioning of the HPA axis is Leukemia Inhibitory Factor (LIF). I propose that OPN may possess a regulatory role in the expression of LIF, with the absence of OPN leading to a greater abundance of LIF mRNA, and consequently, over-production of corticosterone in non-stressful situations. Using the mouse anterior pituitary cell-line AtT-20, a common and highly useful model in HPA axis research, I have found evidence that treatment of these cells with OPN partially inhibits the expression of LIF mRNA. The dose-dependency of this inhibition appears to behave as either positive or negative depending on the cellular density of the culture treated with OPN. Should OPN turn out to be a regulator of LIF mRNA expression, then absence of OPN may lead to an over-abundance of LIF, therefore affecting the expression of several proteins downstream of LIF that potently stimulate corticosterone production, such as the cholesterol transport protein StAR. It may turn out that OPN has an especially significant and indispensable role in the HPA axis via regulation of LIF mRNA levels.
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electronic resource
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vi, 45 p. : ill.
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application/pdf
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Note
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M.S.
Note
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Includes bibliographical references
Note
(type = statement of responsibility)
by Luke Coyle
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Coyle
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Luke
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1983-
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author
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Luke Coyle
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Denhardt
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David T
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chair
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Advisory Committee
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David T Denhardt
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Merrill
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Gary F
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internal member
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Advisory Committee
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Gary F Merrill
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Axelrod
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David E
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internal member
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Advisory Committee
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David E Axelrod
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NamePart
Rutgers University
Role
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degree grantor
Name
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Graduate School - New Brunswick
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school
OriginInfo
DateCreated
(qualifier = exact)
2011
DateOther
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(type = degree)
2011
Place
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xx
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TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier
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ETD
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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/T36T0M9Q
Genre
(authority = ExL-Esploro)
ETD graduate
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Rights
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(ID = rulibRdec0006)
The author owns the copyright to this work.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
RightsHolder
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(type = personal)
Name
FamilyName
Coyle
GivenName
Luke
Role
Copyright Holder
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(AUTHORITY = rulib)
Type
Permission or license
DateTime
2011-01-10 11:31:10
AssociatedEntity
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(AUTHORITY = rulib)
Role
Copyright holder
Name
Luke Coyle
Affiliation
Rutgers University. Graduate School - New Brunswick
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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.
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ETD
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application/pdf
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application/x-tar
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552960
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