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Interleukin-1 mediated cell-type specific signaling in hippocampal neurons and astrocytes
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Huang, Yangyang. Interleukin-1 mediated cell-type specific signaling in hippocampal neurons and astrocytes. Retrieved from https://doi.org/doi:10.7282/T34X57W3

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TitleInterleukin-1 mediated cell-type specific signaling in hippocampal neurons and astrocytes
NameHuang, Yangyang (author); Friedman, Wilma j (chair); Kim, Haesun (internal member); Jonakait, Mill (internal member); Jonakait, G Miller (internal member); Levison, Steve W (outside member); Rutgers University; Graduate School - Newark
Date Created2010
Other Date2010-05 (degree)
SubjectBiology, Interleukin-1, Neurons--Physiology, Astrocytes
Extentv, 97 p. : ill.
DescriptionInterleukin-1β (IL-1β) is a pro-inflammatory cytokine that is implicated in immune and inflammatory responses. In the central nervous system (CNS), IL-1β is synthesized and released during injury, infection, and many neurodegenerative diseases, but also under physiological conditions. Several IL-1-mediated signaling pathways and effects have been identified in hippocampal neurons and astrocytes, but their mechanisms have not been fully defined. IL-1 signaling requires the type one IL-1 receptor (IL-1RI) as well as IL-1 receptor accessory protein (IL-1RAcP) as a receptor partner. A novel isoform of the IL-1 receptor accessory protein, AcPb, has also been found in the CNS, but its role remains unclear. This thesis examined AcPb function in regulating IL-1β signaling. The results showed that IL-1β activated p38 MAPK but not NFκB in neurons. In astrocytes, IL-1β induced both p38 and NFκB pathways in regulating inflammatory responses. AcPb was not involved in mediating either p38 or NFκB in either cell type. In contrast, a physiological level of IL-1β treatment (0.01ng/ml) activated p-Src in neurons via AcPb in vitro. In addition, overexpression of AcPb in astrocytes was sufficient to induce p-Src mediated by IL-1β. Taken together, these results suggest that the restricted expression of AcPb in CNS neurons may mediate neuronal specific IL-1 pathways and outcomes, and that physiological and pathophysiological levels of IL-1β mediate particular neuronal functions via separate pathways.
NotePh.D.
NoteIncludes abstract
NoteIncludes bibliographical references
Noteby Yangyang Huang
Genretheses, ETD doctoral
Persistent URLhttps://doi.org/doi:10.7282/T34X57W3
LanguageEnglish
CollectionGraduate School - Newark Electronic Theses and Dissertations
Organization NameRutgers, The State University of New Jersey
RightsThe author owns the copyright to this work.
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