Interleukin-1 beta induces different gene expression of stromelysin, aggrecan and tumor-necrosis-factor-stimulated gene 6 in human osteoarthritic chondrocytes in vitro

Citation
J. Stove et al., Interleukin-1 beta induces different gene expression of stromelysin, aggrecan and tumor-necrosis-factor-stimulated gene 6 in human osteoarthritic chondrocytes in vitro, PATHOBIOLOG, 68(3), 2000, pp. 144-149
Citations number
25
Categorie Soggetti
Medical Research Diagnosis & Treatment
Journal title
PATHOBIOLOGY
ISSN journal
10152008 → ACNP
Volume
68
Issue
3
Year of publication
2000
Pages
144 - 149
Database
ISI
SICI code
1015-2008(200005/06)68:3<144:IBIDGE>2.0.ZU;2-C
Abstract
Objective: To analyze the gene expression of osteoarthritic chondrocytes cu ltured in alginate after stimulation with interleukin (IL)-1 beta. Methods: Chondrocytes were isolated from osteoarthritic cartilage obtained during t otal knee replacement by sequential enzymatic digestion. After suspension i n alginate, cells were cultured with and without 700 pg/ml IL-1 beta. Quant itative RT-PCR reaction was used to estimate the messenger RNA (mRNA) of th ree different metabolites [tumor-necrosisfactor-stimulated gene 6 (TSG-6), stromelysin-1 (MMP-3) and aggrecan (AGG)]. Results: After having shown the precision of quantitative PCR, this method allowed us to detect IL-1 beta - induced changes in mRNA of TSG-6, MMP-3 and AGG. MMP-3 was found to be the most abundant transcript, IL-1 beta induced a 12-fold upregulation of MMP-3 levels compared to control, and 7-fold of TSG-6. The AGG transcript level, indicating anabolic events, was found to be downregulated by between 2- an d 3-fold. Conclusions: In our culture system, the response of osteoarthriti c chondrocytes to IL-1 beta is preserved. Therefore, this system might be h elpful for further investigation of the influences of drugs, cytokines and growth factors, for example, on the metabolism of chondrocytes at the level of gene transcription as the most basic level of regulation. Copyright (C) 2001 S. Karger AG, Basel.