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Voltage-gated proton channel contributes to secondary damage following spinal cord injury

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TitleInfo
Title
Voltage-gated proton channel contributes to secondary damage following spinal cord injury
Name (type = personal)
NamePart (type = family)
Zheng
NamePart (type = given)
Jiaying
DisplayForm
Jiaying Zheng
Role
RoleTerm (authority = RULIB)
author
Name (type = personal)
NamePart (type = family)
Wu
NamePart (type = given)
Long-Jun
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Long-Jun Wu
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Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Axelrod
NamePart (type = given)
David
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David Axelrod
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Advisory Committee
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internal member
Name (type = personal)
NamePart (type = family)
Xia
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Bing
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Bing Xia
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Advisory Committee
Role
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internal member
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Rutgers University
Role
RoleTerm (authority = RULIB)
degree grantor
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School of Graduate Studies
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school
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Text
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theses
OriginInfo
DateCreated (qualifier = exact)
2018
DateOther (qualifier = exact); (type = degree)
2018-05
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2018
Place
PlaceTerm (type = code)
xx
Language
LanguageTerm (authority = ISO639-2b); (type = code)
eng
Abstract (type = abstract)
Traumatic injury to the spinal cord initiates a series of destructive cellular processes that exacerbate tissue damage at and beyond the original site of injury. These processes include oxidative stress responses and pro-inflammatory cascades that can lead to neuronal loss and demyelination of surviving axons. Previous work in our lab has shown that the voltage-gated proton channel Hv1 is necessary for NADPH oxidase-dependent reactive oxygen species (ROS) production by microglia. This means that Hv1 mediated microglial ROS could be a mechanism to cause neuronal damage under disease conditions. Therefore, we hypothesize that Hv1 contributes to ROS production in microglia after SCI, and loss of function can alleviate secondary injury. To test this, we utilized a moderate spinal cord contusive injury model with adult wild-type and Hv1-/- mice, with the aim of studying the role of Hv1 in microglia activation, ROS production, pro-inflammatory response, neuronal cell death, and demyelination. Our results showed that loss of Hv1 reduced microglial activation following spinal cord injury. Moreover, loss of Hv1 alleviated some of the oxidative stress-mediated secondary injury, as well as inflammatory response. Hv1-/- mice exhibited increased neuronal survival, white matter sparing, and improved locomotive recovery following spinal cord injury. Together, the current study suggested that after spinal cord injury, Hv1 is a potential treatment target to reduce secondary injury.
Subject (authority = RUETD)
Topic
Microbiology and Molecular Genetics
Subject (authority = ETD-LCSH)
Topic
Spinal cord--Wounds and injuries
Subject (authority = ETD-LCSH)
Topic
Microglia
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Rutgers University Electronic Theses and Dissertations
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ETD_8801
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electronic resource
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application/pdf
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Extent
1 online resource (vii, 38 p. : ill.)
Note (type = degree)
M.S.
Note (type = bibliography)
Includes bibliographical references
Note (type = statement of responsibility)
by Jiaying Zheng
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Title
School of Graduate Studies Electronic Theses and Dissertations
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rucore10001600001
Location
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NjNbRU
Identifier (type = doi)
doi:10.7282/T32B92GP
Genre (authority = ExL-Esploro)
ETD graduate
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Rights

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The author owns the copyright to this work.
RightsHolder (type = personal)
Name
FamilyName
Zheng
GivenName
Jiaying
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2018-04-10 14:44:59
AssociatedEntity
Name
jiaying zheng
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Affiliation
Rutgers University. School of Graduate Studies
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Author Agreement License
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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
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2018-05-31
DateTime (encoding = w3cdtf); (qualifier = exact); (point = end)
2020-05-30
Type
Embargo
Detail
Access to this PDF has been restricted at the author's request. It will be publicly available after May 30th, 2020.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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