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dc.contributor.advisorSun, Grace Y.eng
dc.contributor.authorHu, Chunhuaeng
dc.date.issued2007eng
dc.date.submitted2007 Summereng
dc.date.submitted2007 Summereng
dc.description"August 2007."eng
dc.descriptionThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file.eng
dc.descriptionIncludes bibliographical references.eng
dc.descriptionThesis (M.S.) University of Missouri-Columbia 2007.eng
dc.description.abstract[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Reactive oxygen species (ROS) are produced in cells by enzymic and non-enzymic mechanisms and play important roles in the pathogenesis of neurodegenerative diseases. However, mechanisms for the increase in ROS and their effects leading to altered cell metabolism have not been studied in detail in the central nervous system. In the first series of studies, we examined ROS production in primary rat astrocytes and their downstream effects on changes in signaling cascades and morphology using menadione. ROS production induced by menadione was completely inhibited by NADPH oxidase inhibitors including apocynin and gp91ds-tat. Menadione also stimulated phosphorylation of p38 and ERK, and caused actin polymerization and which can be inhibited by inhibitors for NAPDH oxidase and MAPK. In the second part, we tested the role of cytosolic phospholipase A2 in astrocytes in response to oxidative stress. Menadione increased the immunoreactivity of phospho-cPLA2 and caused plasma membranes to become more gel-like, which were abrogated by down regulating cPLA2 with siRNA. In summary, our study demonstrated the important role of NAPDH oxidase in production of ROS and their link to activation of MAPK pathways and cPLA2 in astrocytes. We further demonstrated that excess production of ROS, such as that mediated by menadione, can alter cell membrane properties, morphology, and cytoskeletal arrangement and in turn cell death mechanism.--From public.pdfeng
dc.identifier.merlinb61468575eng
dc.identifier.oclc182537938eng
dc.identifier.urihttps://hdl.handle.net/10355/6270
dc.identifier.urihttps://doi.org/10.32469/10355/6270eng
dc.languageEnglisheng
dc.publisherUniversity of Missouri--Columbiaeng
dc.relation.ispartofcollectionUniversity of Missouri-Columbia. Graduate School. Theses and Dissertationseng
dc.rightsAccess is limited to the campus of the University of Missouri--Columbia.eng
dc.subject.lcshAstrocyteseng
dc.subject.lcshNAD (Coenzyme)eng
dc.subject.lcshApoptosiseng
dc.subject.lcshCell membraneseng
dc.subject.lcshPhospholipase A2 -- Inhibitorseng
dc.subject.lcshCytosoleng
dc.subject.lcshOxidative stresseng
dc.subject.lcshActive oxygeneng
dc.subject.meshAstrocytes -- physiologyeng
dc.subject.meshNADPH Oxidase -- physiologyeng
dc.subject.meshApoptosis -- physiologyeng
dc.subject.meshCell Membraneeng
dc.subject.meshCentral Nervous System -- physiologyeng
dc.subject.meshNADP -- antagonists & inhibitorseng
dc.subject.meshOxidative Stress -- physiologyeng
dc.subject.meshPhospholipases A -- metabolismeng
dc.subject.meshReactive Oxygen Species -- metabolismeng
dc.subject.meshVitamin K3eng
dc.titleActivation of astrocytes: involvement of NADPH oxidase and cytosolic phospholipase A2eng
dc.typeThesiseng
thesis.degree.disciplineNutrition area program (MU)eng
thesis.degree.grantorUniversity of Missouri--Columbiaeng
thesis.degree.levelMasterseng
thesis.degree.nameM.S.eng


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