Abstract:
:Chronic rheumatoid arthritis (RA) is characterized by the hyperplasia of synovial tissue, which results from dysregulation of proliferative and antiapoptotic signals transduced in the synovial cells by unknown mechanisms. To identify candidate factors involved in the regulation of synovial hyperplasia, the expression profile of 205 apoptosis-related genes was compared between tissues from patients with RA and osteoarthritis (OA) using a cDNA microarray. Upregulated genes in the RA synovium included TNFR2, FLICE2, and signaling molecules involved in a MAP kinase pathway (GRB2, MAPK p38). In contrast, genes encoding SARP1 and various cell cycle regulators were down-regulated in the RA synovium relative to OA. Importantly, the expression levels of GRB2 and FLICE2 genes were remarkably enhanced in RA synoviocytes but not in OA synoviocytes in response to tumor necrosis factor (TNF)-alpha treatment. Thus, these results suggest that over-expression of GRB2 and FLICE2 in RA synovium is caused by TNF-alpha inducibility differentially regulated in RA synoviocytes and provide potential pathogenic roles of these genes in the hyperplasia of the RA synovium.
journal_name
Immunol Lettjournal_title
Immunology lettersauthors
Huh SJ,Paik DJ,Chung HS,Youn Jdoi
10.1016/j.imlet.2003.07.002subject
Has Abstractpub_date
2003-12-15 00:00:00pages
93-6issue
2-3eissn
0165-2478issn
1879-0542pii
S0165247803001913journal_volume
90pub_type
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journal_title:Immunology letters
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journal_title:Immunology letters
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journal_title:Immunology letters
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