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J Biol Chem, Vol. 273, Issue 36, 23104-23109, September 4, 1998
,,, and
From the D-type cyclins are induced in
response to mitogens and are essential and rate-limiting for
G1 phase progression in normal mammalian cells. Macrophages
proliferating in response to colony-stimulating factor-1 (CSF-1)
express cyclin D1 and to a lesser extent cyclin D2 but not cyclin D3.
Previously we showed that the macrophage-activating agent
lipopolysaccharide (LPS) blocks CSF-1-induced proliferation and cyclin
D1 expression in macrophages. Here we report upon the effect of LPS on
expression of cyclin D2 in normal mouse bone marrow-derived macrophages
(BMM). Unexpectedly we found that this anti-mitogen raised levels of
CSF-1-stimulated cyclin D2 mRNA and protein. Furthermore, LPS alone
induced cyclin D2 but not cyclin D1. Inhibition of the MEK/ERK
(MAPK/ERK kinase/extracellular signal-regulated kinase)
mitogen-activated protein kinase pathway repressed LPS-induced cyclin
D2 mRNA, whereas inhibition of the p38 mitogen-activated protein
kinase enhanced expression. However, in contrast to cyclin D1, cyclin
D2 in bone marrow-derived macrophages did not appear to be regulated by
protein kinase A pathways. The present data (a) show
elevation of a D-type cyclin in the absence of
proliferation, (b) demonstrate inverse regulation of two
distinct D-type cyclins under identical conditions, and
(c) suggest that cyclin D2 plays a role in macrophage
activation by LPS.
Department of Medicine, University of
Melbourne, Royal Melbourne Hospital, Melbourne, Australia 3050 and
the ¶ Walter and Eliza Hall Institute,
Parkville, Australia 3050
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