Journal article
Reduced severity of experimental autoimmune encephalomyelitis in GMF-deficient mice
Neurochemical research, Vol.32(1), pp.39-47
01/01/2007
DOI: 10.1007/s11064-006-9220-x
Abstract
Glia maturation factor (GMF), a highly conserved brain-specific protein, isolated, sequenced and cloned in our laboratory. Overexpression of GMF in astrocytes induces the production and secretion of granulocyte-macrophage-colony stimulating factor (GM-CSF), and subsequent immune activation of microglia, expression of several proinflammatory genes including major histocompatibility complex proteins, IL-1β, and MIP-1β, all associated with the development of experimental autoimmune encephalomyelitis (EAE), the animal model for multiple sclerosis. Based on GMF’s ability to activate microglia and induce well-established proinflammatory mediators, including GM-CSF, we hypothesize that GMF is involved in the pathogenesis of inflammatory disease EAE. In this present investigation, using GMF-deficient mice, we study the role of GMF and how the lack of GMF affects the EAE disease. Our results show a significant decrease in incidence, delay in onset, and reduced severity of EAE in GMF-deficient mice, and support the hypothesis that GMF plays a major role in the pathogenesis of disease.
Details
- Title: Subtitle
- Reduced severity of experimental autoimmune encephalomyelitis in GMF-deficient mice
- Creators
- Asgar ZaheerSmita ZaheerShailendra K. SahuBaoli Yang - University of IowaRamon Lim
- Resource Type
- Journal article
- Publication Details
- Neurochemical research, Vol.32(1), pp.39-47
- DOI
- 10.1007/s11064-006-9220-x
- ISSN
- 0364-3190
- Language
- English
- Date published
- 01/01/2007
- Academic Unit
- BioVentures Center; Neurology; Obstetrics and Gynecology
- Record Identifier
- 9983557453902771
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