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 Caspase-8 in Oligodendrocyte Development and Mechanisms of Oxidative Injury in Neurons and Glia
  name:
    name part: Thompson, Jeffrey Paul
    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: 2013
    issuance: monographic
  language:
    language term: eng
  physical description:
    form: remote
    extent: 1 online resource (63 pages)
  abstract: Apoptosis is essential not only to the normal development of a multicellular organism but also for the maintenance of tissue homeostasis. This proposal seeks to investigate, in part, the role of oligodendrocyte (OL) apoptosis in myelination. We used an OL-specific conditional knockout animal to study caspase-8 function in OL development; analyzing histological differences in myelination at postnatal day 10 and alterations to OL proliferation, differentiation, and cell death in culture. Our preliminary data suggests that deletion of caspase-8 did not alter OL proliferation or differentiation in culture, but reduced the percentage of apoptotic cells following nutrient deprivation. In vivo, we found an increase in myelinated axons in the spinal cord of caspase-8 deficient mice, indicating a role for caspase-8 in the myelination process. This study also seeks to investigate mechanisms of cell death in OLs, astrocytes, and neurons following oxidative injury. Exposure of primary OLs, astrocytes, and neurons to arachidonic acid (AA) resulted in oxidative stress and cell death. Necrostation-1, the specific inhibitor of receptor interacting protein kinase 1 (RIP-1), markedly prevented AA-induced oxidative death in OLs and astrocytes, but not in neurons. Similarly, we found that blockade of 12-lipoxygenase (LOX) and c-Jun N-terminal kinase (JNK) protected OLs and astrocytes but not neurons against AA toxicity. Consistent with the inability of necrostatin-1 to rescue neurons, we found very low expression of RIP-1 as well as RIP-3 in neurons. Finally, the zinc chelator TPEN effectively abolished AA-induced oxidative death in all three cell types, suggesting zinc release as a common mechanism. Taken together, our findings indicate differences in cell death mechanisms following oxidative injury in astrocytes, OLs, and neurons. The electronic version of this dissertation is accessible from http://hdl.handle.net/1969.1/148320
  note: by Jeffrey Paul Thompson.
  note: "Major Subject: Biomedical Sciences"
  note: Includes vita.
  note: Master of Science Texas A & M University 2012 http://hdl.handle.net/1969.1/148320
  note: Includes bibliographical references.
  note: Text (Thesis)
  subject:
    topic: Major Biomedical Sciences
  subject:
    topic: Necroptosis
  subject:
    topic: RIP-1
  subject:
    topic: Oxidative Stress
  subject:
    topic: Oligodendrocytes
  subject:
    topic: Apoptosis
  identifier: http://hdl.handle.net/1969.1/148320
  record info:
    record content source: TXA
    record creation date: 140113
    record change date: 20151206090952.0
    record identifier: in00003429976
    language of cataloging:
      language term: eng