Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-4-5
pubmed:abstractText
Tumor necrosis factor alpha (TNFalpha) plays a fundamental role in the pathogenesis of wear particle-induced periprosthetic osteolysis. However, particle-induced mechanisms that control TNFalpha gene expression are not yet well characterized. LITAF [lipopolysaccharide (LPS)-induced TNFalpha factor] is a novel transcription factor that regulates expression of the TNFalpha gene, but nothing is known about its role in wear particle-induced osteolysis. We evaluated the effect of titanium aluminum vanadium (TiAlV) and polyethylene particles on mRNA expression of LITAF. A human monocytic leukemia cell line (THP-1) was used in this in vitro study. THP-1 monocytes were differentiated to macrophage-like cells and exposed to LPS-detoxified polyethylene particles and prosthesis-derived TiAlV particles. Supernatant was used for TNFalpha protein measurement and total RNA was extracted from cells. LITAF was analyzed at the mRNA level using semiquantitative RT-PCR. Both polyethylene and TiAlV particles induced significant upregulation of LITAF mRNA that was followed by a significant TNFalpha response. These effects were dependent on the particle dose. Low particle concentrations exhibited no significant effect on expression of TNFalpha and LITAF mRNA. In comparison to exposure to polyethylene and TiAlV particles, LPS stimulation exhibited similar upregulation of LITAF mRNA, but led to an overwhelming TNFalpha response. Our findings provide evidence that LITAF is implicated in the pathogenesis of wear particle-induced osteolysis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0013-5585
pubmed:author
pubmed:issnType
Print
pubmed:volume
52
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
200-7
pubmed:dateRevised
2010-11-5
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Upregulation of LITAF mRNA expression upon exposure to TiAlV and polyethylene wear particles in THP-1 macrophages.
pubmed:affiliation
Department of Orthopedic Surgery, Julius-Maximilians University Würzburg, Würzburg, Germany. b-baumann.klh@mail.uni-wuerzburg.de
pubmed:publicationType
Journal Article