Linked Life Data

10861084

Source:http://linkedlifedata.com/resource/pubmed/id/10861084

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-7-31
pubmed:abstractText
Inflammatory cytokines play a major role in cartilage destruction in diseases such as osteoarthritis and rheumatoid arthritis. Because physical therapies such as continuous passive motion yield beneficial effects on inflamed joints, we examined the intracellular mechanisms of mechanical strain-mediated actions in chondrocytes. By simulating the effects of continuous passive motion with cyclic tensile strain (CTS) on chondrocytes in vitro, we show that CTS is a potent antagonist of IL-1 beta actions and acts as both an anti-inflammatory and a reparative signal. Low magnitude CTS suppresses IL-1 beta-induced mRNA expression of multiple proteins involved in catabolic responses, such as inducible NO synthase, cyclo-oxygenase II, and collagenase. CTS also counteracts cartilage degradation by augmenting mRNA expression for tissue inhibitor of metalloproteases and collagen type II that are inhibited by IL-1 beta. Additionally, CTS augments the reparative process via hyperinduction of aggrecan mRNA expression and abrogation of IL-1 beta-induced suppression of proteoglycan synthesis. Nonetheless, the presence of an inflammatory signal is a prerequisite for the observed CTS actions, as exposure of chondrocytes to CTS alone has little effect on these parameters. Functional analysis suggests that CTS-mediated anti-inflammatory actions are not mediated by IL-1R down-regulation. Moreover, as an effective antagonist of IL-1 beta, the actions of CTS may involve disruption/regulation of signal transduction cascade of IL-1 beta upstream of mRNA transcription. These observations are the first to show that CTS directly acts as an anti-inflammatory signal on chondrocytes and provide a molecular basis for its actions.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
165
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
453-60
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:10861084-Animals, pubmed-meshheading:10861084-Cartilage, Articular, pubmed-meshheading:10861084-Cells, Cultured, pubmed-meshheading:10861084-Chondrocytes, pubmed-meshheading:10861084-Collagen, pubmed-meshheading:10861084-Cyclooxygenase 2, pubmed-meshheading:10861084-Down-Regulation, pubmed-meshheading:10861084-Enzyme Induction, pubmed-meshheading:10861084-Interleukin-1, pubmed-meshheading:10861084-Isoenzymes, pubmed-meshheading:10861084-Knee Joint, pubmed-meshheading:10861084-Matrix Metalloproteinase 1, pubmed-meshheading:10861084-Nitric Oxide Synthase, pubmed-meshheading:10861084-Nitric Oxide Synthase Type II, pubmed-meshheading:10861084-Prostaglandin-Endoperoxide Synthases, pubmed-meshheading:10861084-Proteoglycans, pubmed-meshheading:10861084-Rabbits, pubmed-meshheading:10861084-Stress, Mechanical, pubmed-meshheading:10861084-Tensile Strength, pubmed-meshheading:10861084-Time Factors, pubmed-meshheading:10861084-Tissue Inhibitor of Metalloproteinases
pubmed:year
2000
pubmed:articleTitle
Cyclic tensile strain acts as an antagonist of IL-1 beta actions in chondrocytes.
pubmed:affiliation
Department of Oral and Maxillofacial Surgery, Harvard Medical School, Boston, MA 02115, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't