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J. Cell Biol.,
Volume 144, Number 3, February 8, 1999 427-434
Department of Molecular Genetics, Kumamoto University School of Medicine, Kumamoto 862-0976, Japan
Excess nitric oxide (NO) induces apoptosis
of some cell types, including macrophages. As NO is
synthesized by NO synthase (NOS) from arginine, a
common substrate of arginase, these two enzymes compete for arginine. There are two known isoforms of arginase, types I and II. Using murine macrophage-like
RAW 264.7 cells, we asked if the induction of arginase
II would downregulate NO production and hence
prevent apoptosis. When cells were exposed to lipopolysaccharide (LPS) and interferon-
(IFN-), the
inducible form of NOS (iNOS) was induced, production of NO was elevated, and apoptosis followed. When
dexamethasone and cAMP were further added, both
iNOS and arginase II were induced, NO production
was much decreased, and apoptosis was prevented.
When the cells were transfected with an arginase II expression plasmid and treated with LPS/IFN-, some
cells were rescued from apoptosis. An arginase I expression plasmid was also effective. On the other hand,
transfection with the arginase II plasmid did not prevent apoptosis when a NO donor SNAP or a high concentration (12 mM) of arginine was added. These results indicate that arginase II prevents NO-dependent apoptosis of RAW 264.7 cells by depleting intracellular
arginine and by decreasing NO production.
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