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Instituto de Bioquímica (Centro Mixto Consejo Superior de Investigaciones Cieutí Ficas-Universidad Complutense de Madrid), Facultad de Farmacia, Universidad Complutense, Madrid, Spain
Activation of the macrophage cell line RAW 264.7 with LPS and
IFN-
induces apoptosis through the synthesis of high concentrations
of NO due to the expression of NO synthase-2. In addition to NO,
activated macrophages release other molecules involved in the
inflammatory response, such as reactive oxygen intermediates and PGs.
Treatment of macrophages with cyclopentenone PGs, which are
synthesized late in the inflammatory onset, exerted a negative
regulation on cell activation by impairing the expression of genes
involved in host defense, among them NO synthase-2. However, despite
the attenuation of NO synthesis, the percentage of apoptotic cells
increased with respect to activated cells in the absence of
cyclopentenone PGs. Analysis of the mechanisms by which these PGs
enhanced apoptosis suggested a potentiation of superoxide anion
synthesis that reacted with NO, leading to the formation of higher
concentrations of peroxynitrite, a more reactive and proapoptotic
molecule than the precursors. The effect of the cyclopentenone
15-deoxy-
12,14-PGJ2 on superoxide synthesis
was dependent on p38 mitogen-activated protein kinase activity, but was
independent of the interaction with peroxisomal proliferator-activated
receptor . The potentiation of apoptosis induced by cyclopentenone
PGs involved an increase in the release of cytochrome c
from the mitochondria to the cytosol and in the nitration of this
protein. These results suggest a role for cyclopentenone PGs in the
resolution of inflammation by inducing apoptosis of activated
cells.
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