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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Proliferation-independent induction of macrophage cyclin D2, and repression of cyclin D1, by lipopolysaccharide.

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.[1]


  1. Proliferation-independent induction of macrophage cyclin D2, and repression of cyclin D1, by lipopolysaccharide. Vadiveloo, P.K., Vairo, G., Royston, A.K., Novak, U., Hamilton, J.A. J. Biol. Chem. (1998) [Pubmed]
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