Protein kinase Cα and ζ regulate nitric oxide-induced NF-κB activation that mediates cyclooxygenase-2 expression and apoptosis but not dedifferentiation in articular chondrocytes
被引:48
作者:
Kim, SJ
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h-index: 0
机构:
Kwangju Inst Sci & Technol, Dept Life Sci, Buk Gu, Gwangju 500712, South KoreaKwangju Inst Sci & Technol, Dept Life Sci, Buk Gu, Gwangju 500712, South Korea
Kim, SJ
[1
]
Chun, JS
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h-index: 0
机构:
Kwangju Inst Sci & Technol, Dept Life Sci, Buk Gu, Gwangju 500712, South KoreaKwangju Inst Sci & Technol, Dept Life Sci, Buk Gu, Gwangju 500712, South Korea
Chun, JS
[1
]
机构:
[1] Kwangju Inst Sci & Technol, Dept Life Sci, Buk Gu, Gwangju 500712, South Korea
nitric oxides protein kinase C;
NF-kappa B;
apoptosis;
dedifferentiation;
COX-2;
D O I:
10.1016/S0006-291X(03)00305-X
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Nitric oxide (NO) regulates differentiation, survival, and cyclooxygenase (COX)-2 expression in articular chondrocytes. NO-induced apoptosis and dedifferentiation are mediated by p38 kinase activity and p38 kinase-independent and -dependent inhibition of protein kinase C (PKC)alpha and zeta. Because p38 kinase also activates NF-kappaB, we investigated the functional relationship between PKC and NF-kappaB signaling and the role of NF-kappaB in apoptosis, dedifferentiation, and COX-2 expression. We found that NO-stimulated NF-kappaB activation was inhibited by ectopic PKCalpha and zeta expression, whereas NO-stimulated inhibition of PKCalpha and zeta activity was not affected by NF-kappaB inhibition. Inhibition of NO-induced NF-kappaB activity did not affect inhibition of type II collagen expression but did abrogate COX-2 expression and apoptosis. Taken together, our results indicate that NO-induced inhibition of PKCalpha and activity is required for the NF-kappaB activity that regulates apoptosis and COX-2 expression but not dedifferentiation in articular chondrocytes. (C) 2003 Elsevier Science (USA). All rights reserved.