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Role of beta-endorphin in control of stress and cancer progression in fetal alcohol exposed rats

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TitleInfo
Title
Role of beta-endorphin in control of stress and cancer progression in fetal alcohol exposed rats
Name (type = personal)
NamePart (type = family)
Zhang
NamePart (type = given)
Changqing
NamePart (type = date)
1984-
DisplayForm
Changqing Zhang
Role
RoleTerm (authority = RULIB)
author
Name (type = personal)
NamePart (type = family)
Sarkar
NamePart (type = given)
Dipak K
DisplayForm
Dipak K Sarkar
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
chair
Name (type = personal)
NamePart (type = family)
Cohick
NamePart (type = given)
Wendie S
DisplayForm
Wendie S Cohick
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Bello
NamePart (type = given)
Nicholas T
DisplayForm
Nicholas T Bello
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Thomas
NamePart (type = given)
Paul E
DisplayForm
Paul E Thomas
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 - New Brunswick
Role
RoleTerm (authority = RULIB)
school
TypeOfResource
Text
Genre (authority = marcgt)
theses
OriginInfo
DateCreated (qualifier = exact)
2013
DateOther (qualifier = exact); (type = degree)
2013-10
Place
PlaceTerm (type = code)
xx
Language
LanguageTerm (authority = ISO639-2b); (type = code)
eng
Abstract (type = abstract)
Fetal alcohol exposure causes a series of defects in the animals, including hyper-reactivity to stress, impaired immune function, and increased susceptibility to mammary cancer. Production of β-endorphin (β-EP), the neuronal peptide that is known to inhibit the stress axis, is also reduced in the hypothalamus of fetal alcohol exposed animals. Therefore, we hypothesized that the loss of β-EP neurons in the hypothalamus may be the leading cause of the hyper-reactivity to stress, which then compromises the immune system and leads to increased incidence and progression of mammary cancer. Furthermore, we proposed that enhancement of β-EP neuronal function will have therapeutic effects on treating neoplastic diseases. To test this possibility, we developed two methods that can be used to increase the β-EP neuronal numbers in the hypothalamus: 1) transplantation of in vitro differentiated β-EP neurons into the paraventricular nucleus of the hypothalamus; 2) injection of nanosphere-carried cAMP activating reagents into the third ventricle. Both of these methods were shown to significantly increase the β-EP peptide level in the hypothalamus and significantly decrease the activity of stress axis. By using these methods, we could increase the activities of innate immune cells such as NK cells and macrophages, increase the levels of anti-inflammatory cytokines, and inhibit the growth of carcinogen-induced mammary cancer as well as the metastasis of a mammary carcinoma cell line. These beneficial effects on the control of stress activity, immune function and cancer development caused by increased β-EP production in the hypothalamus could be reversed by treating the animals with naloxone (opioid receptor antagonist), metaproterenol (β-adrenergic receptor agonist), and methyllycaconitine (α7 nicotine acetylcholine receptor antagonist). After β-EP neuronal transplantation, nude rats that lack T-cell-mediated adaptive immune reactivity also showed a significant increase in the ability to resist mammary cancer cell metastasis. These data indicate that the effect of increased hypothalamic β-EP production on mammary cancer growth works through activation of the opioid receptor, inhibition of the sympathetic nervous system, activation of the parasympathetic nervous system, and activation of the innate immune function. In conclusion, measures that activate β-EP neurons in the hypothalamus could inhibit activity of the stress axis, increase innate immune function and inhibit mammary cancer growth and metastasis in both normal and fetal alcohol exposed animals. β-EP neuronal loss caused by fetal alcohol exposure may be an important cause of the hyper-reactive stress axis, decreased immune activity and susceptibility to cancer in the fetal alcohol exposed animals.
Subject (authority = RUETD)
Topic
Animal Sciences
RelatedItem (type = host)
TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier (type = RULIB)
ETD
Identifier
ETD_4990
PhysicalDescription
Form (authority = gmd)
electronic resource
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
xii, 130 p. : ill.
Note (type = degree)
Ph. D.
Note (type = bibliography)
Includes bibliographical references
Note (type = vita)
Includes vita
Note (type = statement of responsibility)
by Changqing Zhang
Subject (authority = ETD-LCSH)
Topic
Endorphins
Subject (authority = ETD-LCSH)
Topic
Rats--Effect of stress on
Subject (authority = ETD-LCSH)
Topic
Alcohol--Physiological effect
Subject (authority = ETD-LCSH)
Topic
Cancer--Etiology
Subject (authority = ETD-LCSH)
Topic
Cancer in animals
RelatedItem (type = host)
TitleInfo
Title
Graduate School - New Brunswick Electronic Theses and Dissertations
Identifier (type = local)
rucore19991600001
Location
PhysicalLocation (authority = marcorg); (displayLabel = Rutgers, The State University of New Jersey)
NjNbRU
Identifier (type = doi)
doi:10.7282/T3XS5SG3
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Rights

RightsDeclaration (ID = rulibRdec0006)
The author owns the copyright to this work.
RightsHolder (type = personal)
Name
FamilyName
Zhang
GivenName
Changqing
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2013-09-10 20:40:25
AssociatedEntity
Name
Changqing Zhang
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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RULTechMD (ID = TECHNICAL1)
ContentModel
ETD
OperatingSystem (VERSION = 5.1)
windows xp
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