Linked Life Data

20595026

Source:http://linkedlifedata.com/resource/pubmed/id/20595026

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2010-7-12
pubmed:abstractText
Zinc-alpha2-glycoprotein (ZAG), a novel adipokine, is downregulated in adipose tissue in obesity, a state characterized by increased adipose tissue macrophage infiltration and chronic low-grade inflammation. This study investigated whether macrophage-secreted factors and TNF-alpha, a major product of macrophages, modulate ZAG expression and secretion by human adipocytes. ZAG was produced primarily by adipocytes, and not by preadipocytes and macrophages. Incubation of preadipocytes with macrophage-conditioned medium for up to 12 days decreased ZAG mRNA and protein release, and the expression of adipogenic markers (PPARgamma and C/EBPalpha). Adipocytes treated with macrophage-conditioned medium for 24h displayed significant reductions in ZAG mRNA and release. Chronic TNF-alpha treatment let to significant decreases in ZAG expression and secretion, but marked upregulation of pro-inflammatory cytokines and chemokines (IL-6, leptin, IL-8, MCP-1 and RANTES) in adipocytes. These findings suggest that macrophage-associated inflammation may play a significant role in the downregulation of ZAG in adipose tissue in obesity.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1872-8057
pubmed:author
pubmed:copyrightInfo
Copyright (c) 2010 Elsevier Ireland Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
30
pubmed:volume
325
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
135-42
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Macrophage-secreted factors inhibit ZAG expression and secretion by human adipocytes.
pubmed:affiliation
Obesity Biology Research Unit, School of Clinical Sciences, University of Liverpool, Liverpool L69 3GA, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't