Linked Life Data

17067317

Source:http://linkedlifedata.com/resource/pubmed/id/17067317

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-10-27
pubmed:abstractText
Glucocorticoid-induced tumour necrosis factor receptor family related protein (GITR) is the 18th member of the tumour necrosis factor receptor superfamily (TNFRSF18) and is known to interact with its cognate ligand GITRL (TNFSF18). We investigated the potential role of GITR in the pro-inflammatory activation of macrophages. Immunohistochemistry and in situ hybridization analyses of human atherosclerotic plaques demonstrated that GITR and its ligand are expressed mainly in lipid-rich macrophages. We then investigated the role of GITR in human and mouse monocyte/macrophage functions. Stimulation of GITR caused nuclear factor (NF)-kappaB-dependent activation of matrix metalloproteinase-9 (MMP-9) and pro-inflammatory cytokine expression in both the human and mouse monocytic/macrophage cell lines, THP-1 and RAW264.7, respectively. These cellular responses were also observed when the THP-1 cells were treated with phorbol-12 myristate-13 acetate (PMA), which is known to induce macrophage differentiation. To demonstrate that these responses are not restricted to cultured cell lines, we tested primary macrophages. Both peritoneal and bone marrow-derived macrophages responded to GITR stimulation with induction of MMP-9 and tumour necrosis factor-alpha (TNF-alpha). Furthermore, the GITR staining pattern overlapped with those of MMP-9 and TNF-alpha in atherosclerotic plaques. These data indicate that GITR-mediated macrophage activation may promote atherogenesis via the induction of pro-atherogenic cytokines/chemokines, and destabilize the atherosclerotic plaques via the induction of the matrix-degrading enzyme, MMP-9.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-10037686, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-10669633, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-11216825, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-11278584, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-11740498, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-11742877, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-11812990, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-11869690, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-14521928, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-14608036, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-14647196, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-14755547, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-14991590, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-15187106, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-15525791, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-15760679, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-16522472, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-1793452, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-3401441, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-8941103, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-9050882, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-9177197, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-9486988, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-9755853, http://linkedlifedata.com/resource/pubmed/commentcorrection/17067317-9887164
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0019-2805
pubmed:author
pubmed:issnType
Print
pubmed:volume
119
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
421-9
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed-meshheading:17067317-Aged, pubmed-meshheading:17067317-Aged, 80 and over, pubmed-meshheading:17067317-Animals, pubmed-meshheading:17067317-Atherosclerosis, pubmed-meshheading:17067317-Carotid Stenosis, pubmed-meshheading:17067317-Cells, Cultured, pubmed-meshheading:17067317-Cytokines, pubmed-meshheading:17067317-Enzyme Activation, pubmed-meshheading:17067317-Glucocorticoid-Induced TNFR-Related Protein, pubmed-meshheading:17067317-Humans, pubmed-meshheading:17067317-Macrophage Activation, pubmed-meshheading:17067317-Matrix Metalloproteinase 9, pubmed-meshheading:17067317-Mice, pubmed-meshheading:17067317-Mice, Inbred ICR, pubmed-meshheading:17067317-Middle Aged, pubmed-meshheading:17067317-NF-kappa B, pubmed-meshheading:17067317-Receptors, Nerve Growth Factor, pubmed-meshheading:17067317-Receptors, Tumor Necrosis Factor, pubmed-meshheading:17067317-Tumor Necrosis Factor-alpha
pubmed:year
2006
pubmed:articleTitle
Glucocorticoid-induced tumour necrosis factor receptor family related protein (GITR) mediates inflammatory activation of macrophages that can destabilize atherosclerotic plaques.
pubmed:affiliation
Department of Genetic Engineering, School of Life Sciences and Biotechnology, Kyungpook National University, Daegu, Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't