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Voltage-gated proton channel contributes to secondary damage following spinal cord injury
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Zheng, Jiaying. Voltage-gated proton channel contributes to secondary damage following spinal cord injury. Retrieved from https://doi.org/doi:10.7282/T32B92GP

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TitleVoltage-gated proton channel contributes to secondary damage following spinal cord injury
NameZheng, Jiaying (author); Wu, Long-Jun (internal member); Axelrod, David (internal member); Xia, Bing (internal member); Rutgers University; School of Graduate Studies
Date Created2018
Other Date2018-05 (degree)
SubjectMicrobiology and Molecular Genetics, Spinal cord--Wounds and injuries, Microglia
Extent1 online resource (vii, 38 p. : ill.)
DescriptionTraumatic 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.
NoteM.S.
NoteIncludes bibliographical references
Noteby Jiaying Zheng
Genretheses, ETD graduate
Persistent URLhttps://doi.org/doi:10.7282/T32B92GP
Languageeng
CollectionSchool of Graduate Studies Electronic Theses and Dissertations
Organization NameRutgers, The State University of New Jersey
RightsThe author owns the copyright to this work.
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