Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-9-11
pubmed:abstractText
Soluble glucocorticoid-induced tumor necrosis factor receptor (sGITR) is a potent stimulator of osteoclastogenesis. The mechanism by which it induces osteoclastogenesis was studied by culturing bone-marrow-derived macrophages (BMM) with conditioned medium from mouse bone marrow stromal cells. GITR and GITR ligand (GITRL) were expressed on the surface of bone marrow stromal cells, and sGITR-induced osteoclastogenesis was inhibited by anti-GITRL Ab, indicating that stimulatory effect of osteoclastogenesis by sGITR involved signaling via GITRL. Bone marrow stromal cells up-regulated cyclooxygenase-2 (COX-2) and produced prostaglandin E(2) (PGE(2)) early in their response to sGITR, and the stimulation of osteoclastogenesis was markedly inhibited by NS398, a COX-2 inhibitor. Later, sGITR markedly reduced the steady-state level of osteoprotegerin (OPG) mRNA and increased receptor activator of nuclear factor-kappaB ligand (RANKL) mRNA. NS398 blocked the sGITR-induced reduction of OPG mRNA but did not significantly affect the sGITR-induced rise in RANKL mRNA. This suggests that down-regulation of OPG by PGE(2) is involved in sGITR-induced osteoclast (OC) formation in the presence of conditioned medium from mouse bone marrow stromal cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, http://linkedlifedata.com/resource/pubmed/chemical/Cyclooxygenase 2, http://linkedlifedata.com/resource/pubmed/chemical/Cyclooxygenase 2 Inhibitors, http://linkedlifedata.com/resource/pubmed/chemical/Glucocorticoid-Induced..., http://linkedlifedata.com/resource/pubmed/chemical/Osteoprotegerin, http://linkedlifedata.com/resource/pubmed/chemical/Prostaglandins E, http://linkedlifedata.com/resource/pubmed/chemical/RANK Ligand, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Nerve Growth Factor, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor, http://linkedlifedata.com/resource/pubmed/chemical/Tnfrsf18 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Tnfsf18 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factors
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
8756-3282
pubmed:author
pubmed:issnType
Print
pubmed:volume
39
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
716-23
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:16750437-Animals, pubmed-meshheading:16750437-Antibodies, pubmed-meshheading:16750437-Bone Marrow Cells, pubmed-meshheading:16750437-Cell Line, pubmed-meshheading:16750437-Cells, Cultured, pubmed-meshheading:16750437-Cyclooxygenase 2, pubmed-meshheading:16750437-Cyclooxygenase 2 Inhibitors, pubmed-meshheading:16750437-Dose-Response Relationship, Drug, pubmed-meshheading:16750437-Down-Regulation, pubmed-meshheading:16750437-Flow Cytometry, pubmed-meshheading:16750437-Gene Expression, pubmed-meshheading:16750437-Glucocorticoid-Induced TNFR-Related Protein, pubmed-meshheading:16750437-Mice, pubmed-meshheading:16750437-Mice, Inbred C57BL, pubmed-meshheading:16750437-Osteoclasts, pubmed-meshheading:16750437-Osteoprotegerin, pubmed-meshheading:16750437-Prostaglandins E, pubmed-meshheading:16750437-RANK Ligand, pubmed-meshheading:16750437-Receptors, Nerve Growth Factor, pubmed-meshheading:16750437-Receptors, Tumor Necrosis Factor, pubmed-meshheading:16750437-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:16750437-Stromal Cells, pubmed-meshheading:16750437-Tumor Necrosis Factors
pubmed:year
2006
pubmed:articleTitle
Soluble glucocorticoid-induced tumor necrosis factor receptor stimulates osteoclastogenesis by down-regulation of osteoprotegerin in bone marrow stromal cells.
pubmed:affiliation
Department of Biological Sciences and the Immunomodulation Research Center, University of Ulsan, Ulsan 680-749, Republic of Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't