About: Macrophages of multiple sclerosis patients display deficient SHP-1 expression and enhanced inflammatory phenotype

Facets (new session)
Description
Metadata
Settings
- owl:sameAs
- Inference Rule:

About: Macrophages of multiple sclerosis patients display deficient SHP-1 expression and enhanced inflammatory phenotype Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Macrophages of multiple sclerosis patients display deficient SHP-1 expression and enhanced inflammatory phenotype
Creator	Jubelt, Burk Panos, Michael Blystone, Scott Christophi, George Christophi, Rebecca Gruber, Ross Hudson, Chad Massa, Paul Mersich, Akos
Source	Medline; PMC
abstract	Recent studies in mice have demonstrated that the protein tyrosine phosphatase SHP-1 is a crucial negative regulator of pro-inflammatory cytokine signaling, TLR signaling, and inflammatory gene expression. Furthermore, mice genetically lacking SHP-1 (me/me) display a profound susceptibility to inflammatory CNS demyelination relative to wild type mice. In particular, SHP-1 deficiency may act predominantly in inflammatory macrophages to increase CNS demyelination as SHP-1-deficient macrophages display co-expression of inflammatory effector molecules and increased demyelinating activity in me/me mice. Recently, we reported that PBMCs of multiple sclerosis (MS) patients have a deficiency in SHP-1 expression relative to normal control subjects indicating that SHP-1 deficiency may play a similar role in MS as to that seen in mice. Therefore, it became essential to examine the specific expression and function of SHP-1 in macrophages from MS patients. Herein, we document that macrophages of MS patients have deficient SHP-1 protein and mRNA expression relative to those of normal control subjects. To examine functional consequences of the lower SHP-1, the activation of STAT6, STAT1, and NF-κB was quantified and macrophages of MS patients showed increased activation of these transcription factors. In accordance with this observation, several STAT6-, STAT1-, and NF-κB-responsive genes that mediate inflammatory demyelination were increased in macrophages of MS patients following cytokine and TLR agonist stimulation. Supporting a direct role of SHP-1 deficiency in altered macrophage function, experimental depletion of SHP-1 in normal subject macrophages resulted in an increased STAT/NF-κB activation and increased inflammatory gene expression to levels seen in macrophages of MS patients. In conclusion, macrophages of MS patients display a deficiency of SHP-1 expression, heightened activation of STAT6, STAT1, and NF-κB and a corresponding inflammatory profile that may be important in controlling macrophage-mediated demyelination in MS.
has issue date	2009-04-27(xsd:dateTime)
bibo:doi	10.1038/labinvest.2009.32
bibo:pmid	19398961
has license	no-cc
sha1sum (hex)	f1e47847b222b58ed3c6cc35c785b1136c388019
schema:url	https://doi.org/10.1038/labinvest.2009.32
resource representing a document's title	Macrophages of multiple sclerosis patients display deficient SHP-1 expression and enhanced inflammatory phenotype
has PubMed Central identifier	PMC2725397
has PubMed identifier	19398961
schema:publication	Lab Invest
resource representing a document's body	covid:f1e47847b222b58ed3c6cc35c785b1136c388019#body_text
is schema:about of	named entity 'SHP-1' named entity 'HAVE' named entity 'CYTOKINE ' named entity 'AGONIST' named entity 'EXPERIMENTAL' named entity 'LOWER' named entity 'DISPLAY' named entity 'DEFICIENCY OF' named entity 'SUBJECT' named entity 'ACTIVITY' named entity 'SUSCEPTIBILITY' named entity 'MACROPHAGE' named entity 'STIMULATION' named entity 'PLAY' named entity 'LACKING' named entity 'INDICATING' named entity 'MULTIPLE SCLEROSIS' named entity 'CNS DEMYELINATION' named entity 'MRNA EXPRESSION' named entity 'ACT' named entity 'TO INCREASE' named entity 'RECENT' named entity 'macrophages' named entity 'controlling' named entity 'mice' named entity 'protein' named entity 'SHP-1' named entity 'macrophages' named entity 'STAT6' named entity 'STAT6' named entity 'TLR' named entity 'macrophages' named entity 'TLR' named entity 'mediate' named entity 'expression' named entity 'SHP-1' named entity 'inflammatory' named entity 'specific' named entity 'stimulation' named entity 'patients' named entity 'relative' named entity 'function' named entity 'demonstrated' named entity 'phenotype' named entity 'Macrophages' named entity 'PATIENTS' named entity 'INFLAMMATORY' named entity 'SPECIFIC' named entity 'PATIENTS' named entity 'WILD TYPE' named entity 'STAT' named entity 'CONCLUSION' named entity 'REPORTED' named entity 'MS.' named entity 'NORMAL' named entity 'SIGNALING' named entity 'NORMAL CONTROL' named entity 'MACROPHAGES' covid:arg/f1e47847b222b58ed3c6cc35c785b1136c388019 named entity 'SHP-1' named entity 'ACCESS' named entity 'ENHANCED' named entity 'PROTEIN TYROSINE PHOSPHATASE SHP-1' named entity 'MEDIATED' named entity 'INCREASED' named entity 'MACROPHAGES' named entity 'CONSEQUENCES' named entity 'PROFILE' named entity 'SUPPORTING' named entity 'CONTROLLING' named entity 'PARTICULAR' named entity 'IMPORTANT' named entity 'SEEN'

Faceted Search & Find service v1.13.91 as of Mar 24 2020

Alternative Linked Data Documents: Sponger | ODE Content Formats:

RDF

ODATA

Microdata

About

OpenLink Virtuoso version 07.20.3229 as of Jul 10 2020, on Linux (x86_64-pc-linux-gnu), Single-Server Edition (94 GB total memory)
Data on this page belongs to its respective rights holders.
Virtuoso Faceted Browser Copyright © 2009-2024 OpenLink Software