NDLI: Interleukin-1β induces death in chondrocyte-like ATDC5 cells through mitochondrial dysfunction and energy depletion in a reactive nitrogen and oxygen species-dependent manner

Content Provider	PubMed Central
Author	Yasuhara, Rika Miyamoto, Yoichi Akaike, Takaaki Akuta, Teruo Nakamura, Masanori Takami, Masamichi Morimura, Naoko Yasu, Kayoko Kamijo, Ryutaro
Copyright Year	2005
Abstract	IL-1 (interleukin-1) acts as a key mediator of the degeneration of articular cartilage in RA (rheumatoid arthritis) and OA (osteoarthritis), where chondrocyte death is observed. It is still controversial, however, whether IL-1 induces chondrocyte death. In the present study, the viability of mouse chondrocyte-like ATDC5 cells was reduced by the treatment with IL-1β for 48 h or longer. IL-1β augmented the expression of the catalytic gp91 subunit of NADPH oxidase, gp91phox, as well as inducible NO synthase in ATDC5 cells. Generation of nitrated guanosine and tyrosine suggested the formation of reactive nitrogen species including ONOO− (peroxynitrite), a reaction product of NO and O2 −, in ATDC5 cells and rat primary chondrocytes treated with IL-1β. Death of ATDC5 cells after IL-1β treatment was prevented by an NADPH-oxidase inhibitor, AEBSF [4-(2-aminoethyl)benzenesulphonyl fluoride], an NO synthase inhibitor, L-NAME (N G-nitro-L-arginine methyl ester), and a ONOO− scavenger, uric acid. The viability of ATDC5 cells was reduced by the ONOO−-generator 3-(4-morpholinyl)sydnonimine hydrochloride, but not by either the NO-donor 1-hydroxy-2-oxo-3-(N-methyl-2-aminopropyl)-3-methyl-1-triazene or S-nitrosoglutathione. Disruption of mitochondrial membrane potential and ATP deprivation were observed in IL-1β-treated ATDC5 cells, both of which were restored by L-NAME, AEBSF or uric acid. On the other hand, no morphological or biochemical signs indicating apoptosis were observed in these cells. These results suggest that the death of chondrocyte-like ATDC5 cells was mediated at least in part by mitochondrial dysfunction and energy depletion through ONOO− formation after IL-1β treatment.
Related Links	http://dx.doi.org/10.1042/bj20041996
Ending Page	323
Page Count	9
Starting Page	315
File Format	PDF
ISSN	02646021
e-ISSN	14708728
Journal	Biochemical Journal
Issue Number	Pt 2
Volume Number	389
Language	English
Publisher	Portland Press Ltd.
Publisher Date	2005-07-15
Access Restriction	Open
Rights Holder	Portland Press Ltd.
Subject Keyword	Cell Biology Biochemistry Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Molecular Biology Biochemistry

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