Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1993-12-20
pubmed:abstractText
Recently, we have shown that a macrophage subpopulation isolated from the synovial tissue of patients with rheumatoid arthritis was potently angiogenic and that a secreted inhibitor of angiogenesis, which is controlled by a tumor suppressor gene in hamster cells, was similar to thrombospondin. In order to investigate the potential role of thrombospondin in human arthritic disorders, we employed immunohistochemistry to examine frozen synovial tissue sections from normal controls (n = 3), patients with rheumatoid arthritis (n = 14) and with osteoarthritis (n = 5). The synovial tissues were stained with monoclonal antibody (mAb) A2.5, which reacts with the heparin-binding domain of thrombospondin, mAb A6.1, which reacts with the epidermal growth factor repeat motif of thrombospondin, and with mAb A4.1, which reacts with the properdin-repeat domain of thrombospondin. In rheumatoid synovial tissues the anti-thrombospondin mAbs reacted with vascular endothelial cells, and to a lesser extent with vascular smooth muscle. Pericytes were stained, particularly with mAb 6.1. Reactivity was also found with isolated macrophages and with the macrophage-derived synovial lining layer in over half the tissues. In osteoarthritis synovial tissues, mAb A2.5 stained fewer macrophages than in rheumatoid arthritis synovial tissues. Slightly fewer blood vessels reacted with mAb A2.5 in normal compared to diseased synovia. The mAbs reacted with capillaries, venules and arterioles in all synovial tissues. We conclude that mAbs to thrombospondin react primarily with blood vessels and macrophages in synovial tissues. Perhaps thrombospondin may function as an adhesive glycoprotein mediating cellular interactions, or it may serve to counteract the effects of the angiogenic factors produced by cells within diseased synovial tissues.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1015-2008
pubmed:author
pubmed:issnType
Print
pubmed:volume
61
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-6
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:8216817-Antibodies, Monoclonal, pubmed-meshheading:8216817-Arterioles, pubmed-meshheading:8216817-Arthritis, Rheumatoid, pubmed-meshheading:8216817-Capillaries, pubmed-meshheading:8216817-Cell Adhesion Molecules, pubmed-meshheading:8216817-Endothelium, Vascular, pubmed-meshheading:8216817-Fibroblasts, pubmed-meshheading:8216817-Humans, pubmed-meshheading:8216817-Immunoenzyme Techniques, pubmed-meshheading:8216817-Immunohistochemistry, pubmed-meshheading:8216817-Inflammation, pubmed-meshheading:8216817-Joint Prosthesis, pubmed-meshheading:8216817-Lymphocytes, pubmed-meshheading:8216817-Macrophages, pubmed-meshheading:8216817-Membrane Glycoproteins, pubmed-meshheading:8216817-Muscle, Smooth, Vascular, pubmed-meshheading:8216817-Osteoarthritis, pubmed-meshheading:8216817-Reference Values, pubmed-meshheading:8216817-Synovial Membrane, pubmed-meshheading:8216817-Thrombospondins, pubmed-meshheading:8216817-Venules
pubmed:year
1993
pubmed:articleTitle
Localization of the angiogenesis inhibitor thrombospondin in human synovial tissues.
pubmed:affiliation
Department of Medicine, Northwestern University Medical School, Chicago, Ill. 60611.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't