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Regulation of gene expression by 17β-estradiol in the arcuate nucleus of the mouse through ERE-dependent and ERE-independent mechanisms

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TypeOfResource
Text
TitleInfo
Title
Regulation of gene expression by 17β-estradiol in the arcuate nucleus of the mouse through ERE-dependent and ERE-independent mechanisms
Identifier (type = pmcid)
PMC4775315
Name (authority = RutgersOrg-Department); (type = corporate)
NamePart
Animal Sciences
Name (authority = RutgersOrg-School); (type = corporate)
NamePart
School of Environmental and Biological Sciences (SEBS)
Genre (authority = RULIB-FS)
Article, Refereed
Genre (authority = NISO JAV)
Accepted Manuscript (AM)
Note (type = peerReview)
Peer reviewed
OriginInfo
DateIssued (encoding = w3cdtf); (keyDate = yes)
2016
Abstract (type = Abstract)
17β-Estradiol (E2) modulates gene expression in the hypothalamic arcuate nucleus (ARC) to control homeostatic functions. In the ARC, estrogen receptor (ER) α is highly expressed and is an important contributor to E2's actions, controlling gene expression through estrogen response element (ERE)-dependent and -independent mechanisms. The objective of this study was to determine if known E2-regulated genes are regulated through these mechanisms. The selected genes have been shown to regulate homeostasis and have been separated into three subsections: channels, receptors, and neuropeptides. To determine if ERE-dependent or ERE-independent mechanisms regulate gene expression, two transgenic mouse models, an ERα knock-out (ERKO) and an ERα knock-in/knock-out (KIKO), which lacks a functional ERE binding domain, were used in addition to their wild-type littermates. Females of all genotypes were ovariectomized and injected with oil or estradiol benzoate (E2B). Our results suggest that E2B regulates multiple genes through these mechanisms. Of note, Cacna1g and Kcnmb1 channel expression was increased by E2B in WT females only, suggesting an ERE-dependent regulation. Furthermore, the NKB receptor, Tac3r, was suppressed by E2B in WT and KIKO females but not ERKO females, suggesting that ERα-dependent, ERE-independent signaling is necessary for Tac3r regulation. The adrenergic receptor Adra1b was suppressed by E2B in all genotypes indicating that ERα is not the primary receptor for E2B's actions. The neuropeptide Tac2 was suppressed by E2B through ERE-dependent mechanisms. These results indicate that E2B activates both ERα-dependent and independent signaling in the ARC through ERE-dependent and ERE-independent mechanisms to control gene expression.
Language
LanguageTerm (authority = ISO 639-3:2007); (type = text)
English
PhysicalDescription
InternetMediaType
application/pdf
Extent
39 p.
Extension
DescriptiveEvent
Type
Citation
DateTime (encoding = w3cdtf)
2016
AssociatedObject
Name
Steroids
Type
Journal
Relationship
Has part
Detail
128-138
Identifier (type = volume and issue)
107
Reference (type = url)
http://dx.doi.org/10.1016/j.steroids.2016.01.003
Extension
DescriptiveEvent
Type
Grant award
AssociatedEntity
Role
Funder
Name
National Institutes of Health
AssociatedEntity
Role
Originator
Name
Troy A. Roepke
AssociatedObject
Type
Grant number
Name
R00DK083457
Subject (authority = local)
Topic
17β-Estradiol
Subject (authority = local)
Topic
Ovariectomy
Subject (authority = local)
Topic
ERα
Subject (authority = local)
Topic
Arcuate nucleus
Name (type = personal)
NamePart (type = family)
Yang
NamePart (type = given)
Jennifer A.
Affiliation
Animal Sciences, Rutgers University
Role
RoleTerm (authority = marcrt); (type = text)
author
Name (type = personal)
NamePart (type = family)
Mamounis
NamePart (type = given)
Kyle
Affiliation
Animal Sciences, Rutgers University
Role
RoleTerm (authority = marcrt); (type = text)
author
Name (type = personal)
NamePart (type = family)
Yasrebi
NamePart (type = given)
Ali
Affiliation
Animal Sciences, Rutgers University
Role
RoleTerm (authority = marcrt); (type = text)
author
Name (authority = orcid); (authorityURI = http://id.loc.gov/vocabulary/identifiers/orcid.html); (type = personal); (valueURI = http://orcid.org/0000-0001-5426-2266)
NamePart (type = family)
Roepke
NamePart (type = given)
Troy A.
Affiliation
Animal Sciences, Rutgers University
Role
RoleTerm (authority = marcrt); (type = text)
author
RelatedItem (type = host)
TitleInfo
Title
Roepke, Troy A.
Identifier (type = local)
rucore30176800001
RelatedItem (type = host)
TitleInfo
Title
Yang, Jennifer A.
Identifier (type = local)
rucore30190600001
RelatedItem (type = host)
TitleInfo
Title
Mamounis, Kyle J.
Identifier (type = local)
rucore30196300001
RelatedItem (type = host)
TitleInfo
Title
Yasrebi, Ali
Identifier (type = local)
rucore30190700001
Location
PhysicalLocation (authority = marcorg); (displayLabel = Rutgers, The State University of New Jersey)
NjNbRU
Identifier (type = doi)
doi:10.7282/T3G44SMX
Genre (authority = ExL-Esploro)
Accepted Manuscript
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RightsDeclaration (AUTHORITY = FS); (ID = rulibRdec0004)
Copyright for scholarly resources published in RUcore is retained by the copyright holder. By virtue of its appearance in this open access medium, you are free to use this resource, with proper attribution, in educational and other non-commercial settings. Other uses, such as reproduction or republication, may require the permission of the copyright holder.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
RightsEvent
Type
Permission or license
AssociatedObject
Type
License
Name
Multiple author license v. 1
Detail
I hereby grant to Rutgers, The State University of New Jersey (Rutgers) the non-exclusive right to retain, reproduce, and distribute the deposited work (Work) in whole or in part, in and from its electronic format, without fee. This agreement does not represent a transfer of copyright to Rutgers.Rutgers may make and keep more than one copy of the Work for purposes of security, backup, preservation, and access and may migrate the Work to any medium or format for the purpose of preservation and access in the future. Rutgers will not make any alteration, other than as allowed by this agreement, to the Work.I represent and warrant to Rutgers that the Work is my original work. I also represent that the Work does not, to the best of my knowledge, infringe or violate any rights of others.I further represent and warrant that I have obtained all necessary rights to permit Rutgers to reproduce and distribute the Work and that any third-party owned content is clearly identified and acknowledged within the Work.By granting this license, I acknowledge that I have read and agreed to the terms of this agreement and all related RUcore and Rutgers policies.
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ContentModel
Document
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1.6
DateCreated (point = end); (encoding = w3cdtf); (qualifier = exact)
2015-12-29T16:41:48
DateCreated (point = end); (encoding = w3cdtf); (qualifier = exact)
2017-02-13T16:30:19
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