Identification of Human Semaphorin E Gene Expression in Rheumatoid Synovial Cells by mRNA Differential Display

Rheumatoid arthritis (RA) is characterised by chronic inflammation of synovial tissue with aggressive proliferation of synovial cells causing destruction of cartilage and bone. Immunopathological mechanisms, infectious causes and genetic factors have been discussed, but the etiology of the disease h...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 1997-05, Vol.234 (1), p.153-156
Main Authors: Mangasser-Stephan, Kerstin, Dooley, Steven, Welter, Cornelius, Mutschler, Wolf, Hanselmann, Rainer G.
Format: Article
Language:English
Subjects:
Arthritis, Rheumatoid - etiology
Arthritis, Rheumatoid - genetics
Blotting, Northern
Cells, Cultured
Cloning, Molecular
DNA, Complementary - chemistry
Electrophoresis, Agar Gel
Gene Expression Regulation
Humans
Membrane Proteins - genetics
Molecular Sequence Data
Nerve Tissue Proteins - genetics
RNA, Messenger - genetics
Sequence Analysis
Synovial Membrane - metabolism
Up-Regulation
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Summary:Rheumatoid arthritis (RA) is characterised by chronic inflammation of synovial tissue with aggressive proliferation of synovial cells causing destruction of cartilage and bone. Immunopathological mechanisms, infectious causes and genetic factors have been discussed, but the etiology of the disease has not been understood until now. Especially, the mechanisms driving tumourlike growth and invasive behaviour of fibroblastoid synovial cells have not been identified yet. Our aim is to find cellular factors which are mediators for such pathways. One possibility to approach this, is searching for disease-relevant genes. We applied the mRNA-differential display technique to compare mRNA expression patterns of normal and rheumatic synovial fibroblasts. We identified an upregulation of the human semaphorin E gene in rheumatoid synovial fibroblastoid cells. Interestingly semaphorin E is a member of a protein-family described to play an immunosuppressive role via inhibition cytokines. A relevance of this finding towards the pathogenesis of RA is discussed.
ISSN:0006-291X
1090-2104
DOI:10.1006/bbrc.1997.6607