Effects of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) on the expression of inflammatory cytokines and apoptosis induction in rheumatoid synovial fibroblasts and monocytes
- Authors
- Ji, JD; Cheon, H; Jun, JB; Choi, SJ; Kim, YR; Lee, YH; Kim, TH; Chae, IJ; Song, GG; Yoo, DH; Kim, SY; Sohn, J
- Issue Date
- 11월-2001
- Publisher
- ACADEMIC PRESS LTD
- Keywords
- Apoptosis; Inflammatory cytokine; NF-κB; PPAR-γ; Rheumatoid arthritis
- Citation
- JOURNAL OF AUTOIMMUNITY, v.17, no.3, pp.215 - 221
- Indexed
- SCIE
SCOPUS
- Journal Title
- JOURNAL OF AUTOIMMUNITY
- Volume
- 17
- Number
- 3
- Start Page
- 215
- End Page
- 221
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/123628
- DOI
- 10.1006/jaut.2001.0542
- ISSN
- 0896-8411
- Abstract
- This study was performed to investigate whether peroxisome proliterator-activated receptor-gamma (PPAR-gamma) exerted an anti-inflammatory effect on rheumatoid synovial cells and inhibited dysregulated proliferation. The expression of PPAR-gamma mRNA in cultured human synoviocytes and THP-1 cells was analysed by RT-PCR. PPAR-gamma was expressed in normal, osteoarthritis (OA), rheumatoid arthritis (RA) synovial cells as well as a human monocytic cell line, THP-1. In RA and OA synoviocytes, the induction of inflammatory cytokine mRNA expression such as TNF-a and IL-1 beta was significantly inhibited by the natural PPAR-gamma agonist 15 deoxy-Delta (12,14) prostaglandin J(2), (15d-PGJ,). The effect of PPAR-y on the nuclear factor (NF)-KB activity was tested by electrophoretic mobility shift assay (EMSA). Both troglitazone and 15d-PGJ(2) markedly inhibited TNF-a-induced NF-KB activation at 30 muM. However, PPAR-y agonist neither reduced proliferation nor induced apoptosis in RA synoviocytes when measured by XTT assay and fluorescence activated cell sorter (FACS) analysis. In contrast, it induced apoptosis in a dose-dependent manner in THP-1 cells and augmented INF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis as well. In conclusion, these data demonstrate that PPAR-gamma is expressed in human synoviocytes and THP-1 cells, and the PPAR-7 activation inhibits expression of inflammatory cytokines in RA synoviocytes. Furthermore, PPAR-y activation induces apoptosis by itself and augments TRAIL/ Apo2L-induced apoptosis in THP-1 cells. These results suggest that PPAR-7 agonists may provide a new therapeutic approach for RA. (C) 2001 Academic Press.
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