title: Enhanced expression of glia maturation factor correlates with glial activation in the brain of triple transgenic Alzheimer's disease mice.
abstract: We previously demonstrated that glia maturation factor (GMF), a brain specific protein, isolated, sequenced and cloned in our laboratory, induce expression of proinflammatory cytokines and chemokines in the central nervous system. We also reported that the up-regulation of GMF in astrocytes leads to the destruction of neurons suggesting a novel pathway of GMF-mediated cytotoxicity of brain cells, and implicated its involvement in the pathogenesis of inflammatory neurodegenerative diseases. In the present study, we examined the expressions of GMF in triple-transgenic Alzheimer's disease (3xTg-AD) mice. Our results show a 13-fold up-regulation of GMF and 8-12-fold up-regulation of proinflammatory cytokines tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), IL-1β, interferon gamma (IFN-γ), and chemokine (C-C motif) ligand 2 (CCL2) and C-X-C motif chemokine 10 (CXCL10/IP-10) mRNA as determined by quantitative real-time RT-PCR in the brain of 3xTg-AD mice as compared to non-transgenic (Non-Tg) mice. In conclusion, the increase in GMF and cytokine/chemokine expression was correlated with reactive glial fibrillary acidic protein positive astrocytes and ionized calcium binding adaptor molecule 1 (Iba-1)-positive microglia in 3xTg-AD mice.
authors.affiliation: Department of Neurology, The University of Iowa, 200 Hawkins Drive, Iowa City, IA 52242, USA.
authors.forename: Smita
authors.initials: S
authors.lastname: Zaheer
authors.forename: Ramasamy
authors.initials: R
authors.lastname: Thangavel
authors.forename: Yanghong
authors.initials: Y
authors.lastname: Wu
authors.forename: Mohammad Moshahid
authors.initials: MM
authors.lastname: Khan
authors.forename: Duraisamy
authors.initials: D
authors.lastname: Kempuraj
authors.forename: Asgar
authors.initials: A
authors.lastname: Zaheer
mesh_terms: D000544:Alzheimer Disease / Q000235:genetics* / Q000378:metabolism* / Q000523:psychology; D016564:Amyloid beta-Protein Precursor / Q000235:genetics; D000818:Animals; D015153:Blotting, Western; D001921:Brain / Q000276:immunology*; D001927:Brain Diseases / Q000235:genetics / Q000473:pathology; D018925:Chemokines / Q000096:biosynthesis; D003072:Cognition Disorders / Q000235:genetics / Q000523:psychology; D016207:Cytokines / Q000096:biosynthesis; D004797:Enzyme-Linked Immunosorbent Assay; D005455:Fluorescent Antibody Technique; D020904:Glia Maturation Factor / Q000096:biosynthesis*; D006801:Humans; D007150:Immunohistochemistry; D017774:Long-Term Potentiation / Q000235:genetics / Q000502:physiology; D008262:Macrophage Activation / Q000235:genetics*; D051379:Mice; D008822:Mice, Transgenic; D016874:Neurofibrillary Tangles / Q000235:genetics / Q000473:pathology; D009457:Neuroglia / Q000276:immunology / Q000502:physiology*; D009473:Neuronal Plasticity / Q000235:genetics / Q000502:physiology; D058225:Plaque, Amyloid / Q000235:genetics / Q000473:pathology; D053764:Presenilin-1 / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D016875:tau Proteins / Q000235:genetics
chemical_list: D016564:Amyloid beta-Protein Precursor; D018925:Chemokines; D016207:Cytokines; D020904:Glia Maturation Factor; D053764:Presenilin-1; D016875:tau Proteins