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Papers In Press, published online ahead of print August 7, 2003
Department of Life Science, Kwangju Institute of Science and Tecnology, Gwangju 500-712
Corresponding Author: jschun{at}kjist.ac.kr
Nitric oxide (NO) in articular chondrocytes regulates differentiation, survival and inflammatory responses by modulating extracellular signal-regulated protein kinase (ERK)-1 and -2, p38 kinase and protein kinase C (PKC)
J. Biol. Chem, 10.1074/jbc.M304887200
Submitted on May 9, 2003
Revised on August 7, 2003
Accepted on August 7, 2003
Actin cytoskeletal architecture regulates nitric oxide-induced apoptosis, dedifferentiation and cyclooxygenase-2 expression in articular chondrocytes via mitogen-activated protein kinase and protein kinase C pathways
and 
. In this study, we investigated the effects of the actin cytoskeletal architecture on NO-induced dedifferentiation, apoptosis, cyclooxygenase (COX)-2 expression and prostaglandin E2 (PGE2) production in articular chondrocytes, with a focus on ERK-1/-2, p38 kinase and PKC signaling. Disruption of the actin cytoskeleton by cytochalasin D (CD) inhibited NO-induced apoptosis, dedifferentiation, COX-2 expression and PGE2 production in chondrocytes cultured on plastic or during cartilage explants culture. CD treatment did not affect ERK-1/-2 activation, but blocked the signaling events necessary for NO-induced dedifferentiation, apoptosis, and COX-2 expression such as activation of p38 kinase and inhibition of PKC and . CD also suppressed activation of downstream signaling of p38 kinase and PKC, such as NF-
B activation, p53 accumulation, and caspase-3 activation, which are necessary for NO-induced apoptosis. NO production in articular chondrocytes caused down regulation of phosphatidylinositol (PI) 3-kinase and Akt activities. The down regulation of PI-3 kinase and Akt was blocked by CD treatment, and the CD effects on apoptosis, p38 kinase, and PKC and were abolished by the inhibition of PI-3 kinase with LY294002. Our results collectively indicate that the actin cytoskeleton mediates NO-induced regulatory effects in chondrocytes by modulating down regulation of PI-3 kinase and Akt, activation of p38 kinase, and inhibition of PKC and .
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