Linked Life Data

21437966

Source:http://linkedlifedata.com/resource/pubmed/id/21437966

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2011-7-12
pubmed:abstractText
Catabolic inflammatory cytokines are prevalent in osteoarthritis (OA). The purpose of this study was to evaluate an autologous protein solution (APS) as a potential chondroprotective agent for OA therapy. APS was prepared from platelet-rich plasma (PRP). The APS solution contained both anabolic (bFGF, TGF-?1, TGF-?2, EGF, IGF-1, PDGF-AB, PDGF-BB, and VEGF) and anti-inflammatory (IL-1ra, sTNF-RI, sTNF-RII, IL-4, IL-10, IL-13, and IFN?) cytokines but low concentrations of catabolic cytokines (IL-1?, IL-1?, TNF?, IL-6, IL-8, IL-17, and IL-18). Human articular chondrocytes were pre-incubated with the antagonists IL-1ra, sTNF-RI, or APS prior to the addition of recombinant human IL-1? or TNF?. Following exposure to inflammatory cytokines, the levels of MMP-13 in the culture medium were evaluated by ELISA. MMP-13 production stimulated in chondrocytes by IL-1? or TNF? was reduced by rhIL-1ra and sTNF-RI to near basal levels. APS was also capable of inhibiting the production of MMP-13 induced by both IL-1? and TNF?. The combination of anabolic and anti-inflammatory cytokines in the APS created from PRP may render this formulation to be a potential candidate for the treatment of inflammation in patients at early stages of OA.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1554-527X
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 Orthopaedic Research Society.
pubmed:issnType
Electronic
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1320-6
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Autologous protein solution inhibits MMP-13 production by IL-1? and TNF?-stimulated human articular chondrocytes.
pubmed:affiliation
Biomet Biologics, Warsaw, Indiana. jennifer.woodell-may@biomet.com
pubmed:publicationType
Journal Article