Reference : TNF-alpha protects human primary articular chondrocytes from nitric oxide-induced apo...
Scientific journals : Article
Human health sciences : Rheumatology
http://hdl.handle.net/2268/94573
TNF-alpha protects human primary articular chondrocytes from nitric oxide-induced apoptosis via nuclear factor-kappaB
English
Relic, Biserka [Université de Liège - ULg > > Rhumatologie >]
Bentires-Alj, Mohamed [ > > ]
Ribbens, Clio mailto [Université de Liège - ULg > > Rhumatologie >]
Franchimont, Nathalie [ > > ]
Guerne, Pierre-Andre [ > > ]
Benoit, Valerie [ > > ]
Merville, Marie-Paule mailto [Université de Liège - ULg > Département de pharmacie > Chimie médicale >]
Bours, Vincent mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > GIGA-R : Génétique générale et humaine >]
Malaise, Michel mailto [Université de Liège - ULg > Département des sciences cliniques > Rhumatologie >]
2002
Laboratory Investigation : Journal of Technical Methods & Pathology
Lippincott Williams & Wilkins
82
12
1661-1672
Yes (verified by ORBi)
International
0023-6837
1530-0307
Hagerstown
MD
[en] Anti-Infective Agents ; Chromones ; Enzyme Inhibitors ; Isoenzymes ; Membrane Proteins ; Morpholines ; NF-kappa B ; Nitric Oxide Donors ; Tumor Necrosis Factor-alph
[en] TNF-alpha plays a key role in rheumatoid arthritis, but its effect on chondrocyte
survival is still conflicting. In the present study, we tested how TNF-alpha
influences chondrocyte survival in response to nitric oxide (NO)-related
apoptotic signals, which are abundant during rheumatoid arthritis. Human primary
articular chondrocytes or cartilage explants were pretreated with TNF-alpha for
24 hours and then treated with the proapoptotic NO donor sodium-nitro-prusside
(SNP) for an additional 24 hours. TNF-alpha pretreatment markedly protected
chondrocytes from SNP-induced cell death. Preincubation of chondrocytes with
TNF-alpha inhibited both SNP-induced high-molecular weight DNA fragmentation and
annexin V-FITC binding. Of interest, TNF-alpha induced persistent nuclear
factor-kappaB (NF-kappaB)-DNA binding activity even in the presence of SNP,
mirroring apoptosis protection effects. Both the TNF-alpha antiapoptotic effect
and NF-kappaB-DNA binding activity were significantly inhibited by NF-kappaB
inhibitors, Bay 11-7085, MG-132, and adenovirus-expressing mutated IkappaB-alpha.
Phosphatidylinositol-3 kinase inhibitor LY 294002 also markedly inhibited the
antiapoptotic effect of TNF-alpha. In primary chondrocytes, TNF-alpha induced
expression of the antiapoptotic protein Cox-2, which persisted in the presence of
SNP, and a specific Cox-2 inhibitor significantly blocked the TNF-alpha
protective effect. We therefore conclude that TNF-alpha-mediated protection of
chondrocytes from NO-induced apoptosis acts through NF-kappaB and requires Cox-2
activity.
Researchers ; Professionals
http://hdl.handle.net/2268/94573

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