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J. Biol. Chem., Vol. 277, Issue 33, 29681-29685, August 16, 2002
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From the Unité de Recherche Stéroïdes et
Système Nerveux, Unité 488 de l'Institut National de la
Santé et de la Recherche Médicale (INSERM), 80 avenue du
Général Leclerc, 94276 Le
Kremlin-Bicêtre, France
15-Deoxy-
MAP Kinase Cascades Are Activated in Astrocytes and Preadipocytes
by 15-Deoxy-
12-14-prostaglandin J2 and the
Thiazolidinedione Ciglitazone through Peroxisome Proliferator Activator
Receptor 
-independent Mechanisms Involving Reactive
Oxygenated Species*
12-14-prostaglandin
J2 (dPGJ2) and thiazolidinediones are known as ligands for
the peroxisome proliferator activator receptor 
(PPAR) a member
of the nuclear receptor superfamily. Herein, we show that dPGJ2
activates, in cultured primary astrocytes, Erk, Jnk, p38 MAP kinase,
and ASK1, a MAP kinase kinase kinase, which can be involved in the
activation of Jnk and p38 MAP kinase. The activation kinetic is similar
for the three MAP kinase. The activation of the MAP kinases is
detectable around 0.5 h. The activation increases with dPGJ2 in a
dose dependent manner (0-15 µM). A scavenger of reactive
oxygenated species (ROS), N-acetylcysteine (NAC) at 20 mM, completely suppresses the activation of MAP kinases and
ASK1, suggesting a role for oxidative stress in the activation mechanism. Other prostaglandin cyclopentenones than dPGJ2,
A2, and to a lesser degree, A1 also stimulate
the MAP kinases, although they do not bind to PPAR. Ciglitazone (20 µM), a thiazolidinedione that mimics several effects of
dPGJ2 in different cell types, also activates the three MAP kinase
families and ASK1 in cultured astrocytes. However the activation is
more rapid (it is detectable at 0.25 h) and more sustained (it is
still strong after 4 h). NAC prevents the activation of the three
MAP kinase families by ciglitazone. Another thiazolidinedione that
binds to PPAR, rosiglitazone, does not activate MAP kinases,
indicating that the effect of ciglitazone on MAP kinases is independent
of PPAR . Ciglitazone and less strongly dPGJ2 activate Erk in
undifferentiated cells of the adipocyte cell line 1B8. Ciglitazone also
activates Jnk and p38 MAP kinase in these preadipocytes. Our findings
suggest that a part of the biological effects of dPGJ2 and ciglitazone
involve the activation of the three MAP kinase families probably
through PPAR-independent mechanisms involving ROS.
*
This work was supported by the "Association pour la
Recherche contre le Cancer" (Grants 6624 and 9854 (to M. P.)), the
CNRS, and the University Paris XI.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed. Tel.:
33-1-49-59-18-34; Fax: 33-1-45-21-19-40; E-mail:
pierre@kb.inserm.fr.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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