rdf-syntax-grammar
mods:
  schema location: http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-2.xsd
  title info:
    non sort: The
    title: Role of RIP3 in Neuroinflammation in the Postnatal Mouse Brain
  name:
    name part: Gillis, David C.
    role:
      role term: creator
    role:
      role term: author.
  name:
    name part: Li, Jianrong
    role:
      role term: thesis advisor.
  name:
    name part: Texas A & M University
    role:
      role term: degree granting institution.
  type of resource: text
  genre: bibliography
  origin info:
    place:
      place term: txu
    date issued: 2015
    issuance: monographic
  language:
    language term: eng
  physical description:
    form: remote
    extent: 1 online resource.
  abstract: Inflammation in the developing central nervous system (CNS) can contribute to numerous issues in the fully developed adult. Uncovering pathways responsible for the inflammation is valuable for future intervention strategies aimed at preventing or reducing inflammation. Receptor interacting protein kinase 3 (RIP3) has recently been identified as a critical signaling molecule in initiating programmed necrosis (also termed necroptosis), which may contribute to cell damage and subsequent inflammation under pathophysiological conditions such as stroke and traumatic injury. The goal of this study was to use genetic approaches to determine the role of RIP3 in brain immune responses after systemic inflammatory challenge and the contribution of RIP3 to inflammation-induced potentiation of hippocampal injury in an ex vivo model of hypoxia/ischemia. Stimulation with lipopolysaccharide (LPS) elicited robust proinflammatory responses of organotypic hippocampal slices and significantly exacerbated CA1 neuronal excitotoxicity after subsequent oxygen glucose deprivation (OGD). Genetic ablation of RIP3 resulted in decreased levels of interleukin-1[lowercase beta symbol] (IL-1[lowercase beta symbol]) after LPS stimulation and suppressed excitotoxicity after subsequent OGD challenge. These results suggest that activation of RIP3 increases proinflammatory responses in cultured hippocampal slices. To determine if RIP3 regulates inflammation in vivo, we examined cytokine and chemokine levels of the brain after subcutaneous LPS administration followed by hypoxia in early postnatal pups. Mice lacking RIP3 produced significantly lower levels of proinflammatory cytokine IL-1[lowercase beta symbol] 6-24 hours after LPS administration when compared to wildtype RIP3^+/+ littermates. In contrast, 4 and 21 days after LPS administration followed by hypoxia, IL-1[lowercase beta symbol] and other proinflammatory cytokine transcript levels in the brain were drastically diminished and were comparable …
  note: by David C. Gillis.
  note: "Major Subject: Biomedical Sciences"
  note: Includes vita.
  note: Master of Science Texas A & M University 2015 http://hdl.handle.net/1969.1/155480
  note: Includes bibliographical references.
  note: Text (Thesis)
  subject:
    topic: Major Biomedical Sciences
  subject:
    topic: RIP3
  subject:
    topic: Neuroinflammation
  subject:
    topic: LPS
  subject:
    topic: Programmed cell death
  identifier: http://hdl.handle.net/1969.1/155480
  record info:
    record content source: TXA
    record creation date: 160909
    record change date: 20170926144552.0
    record identifier: in00003738314
    language of cataloging:
      language term: eng