Linked Life Data

17551829

Source:http://linkedlifedata.com/resource/pubmed/id/17551829

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2007-11-2
pubmed:abstractText
Inflammatory cytokines are implemented in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. We previously demonstrated that glia maturation factor (GMF), a brain protein, isolated, sequenced and cloned in our laboratory, induce expression of proinflammatory cytokine/chemokine in the central nervous system (CNS). We found GMF-deficient (knockout) mice relatively resistant to EAE development after immunization with encephalitogenic MOG peptide 35-55. Consistent with these findings, the expression of proinflammatory cytokines in CNS of mice with EAE differed profoundly between wild type and GMF-knockout mice. In the present study we examined the expressions of six murine signal transducers and activators of transcription (STATs) genes, which are known to regulate the cytokine-dependent signal transduction pathways in autoimmune inflammation. The expressions of STATs genes were evaluated in the brains and spinal cords of wild type and GMF-knockout mice at the peak of EAE by quantitative real-time RT-PCR. Compared to GMF-knockout mice, the expressions of STAT1, STAT2, STAT3, STAT4, STAT5, and STAT6 genes were significantly (P < 0.001) upregulated in the wild type mice exhibiting EAE symptoms. The results are consistent with the diminished development of EAE in the GMF-knockout mice. A significant suppression of STATs expression in GMF-knockout mice suggests GMF as an upstream effector of JAK/STAT signaling.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0364-3190
pubmed:author
pubmed:issnType
Print
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2123-31
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:17551829-Animals, pubmed-meshheading:17551829-Blotting, Western, pubmed-meshheading:17551829-Cytokines, pubmed-meshheading:17551829-Encephalomyelitis, Autoimmune, Experimental, pubmed-meshheading:17551829-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:17551829-Glia Maturation Factor, pubmed-meshheading:17551829-Immunoprecipitation, pubmed-meshheading:17551829-Janus Kinases, pubmed-meshheading:17551829-Mice, pubmed-meshheading:17551829-Mice, Knockout, pubmed-meshheading:17551829-Myelin Sheath, pubmed-meshheading:17551829-Phosphorylation, pubmed-meshheading:17551829-RNA, Messenger, pubmed-meshheading:17551829-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:17551829-STAT Transcription Factors, pubmed-meshheading:17551829-Signal Transduction, pubmed-meshheading:17551829-Suppressor of Cytokine Signaling Proteins
pubmed:year
2007
pubmed:articleTitle
Glia maturation factor regulation of STAT expression: a novel mechanism in experimental autoimmune encephalomyelitis.
pubmed:affiliation
Veterans Affairs Medical Center, Iowa City, IA, USA. asgar-zaheer@uiowa.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, N.I.H., Extramural