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

Vadiveloo, PK; Vairo, G; Royston, AK; Novak, U; Hamilton, JA

Author(s): Vadiveloo, PK; Vairo, G; Royston, AK; Novak, U; Hamilton, JA;
Details: Publication Year 1998-09-04,Volume 273,Issue #36,Page 23104-23109
Journal Title: JOURNAL OF BIOLOGICAL CHEMISTRY
Publication Type: Journal Article
Abstract: D-type cyclins are induced in response to mitogens and are essential, and rate-limiting for G(1) 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 me found that this anti-mitogen raised levels of CSF-1-stimulated cyclin D2 mRNA and protein. Furthermore, LPS alone induced cyclin Ha 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.
Publisher: AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
Keywords: NECROSIS-FACTOR-ALPHA; STIMULATING FACTOR-I; CELL-CYCLE; GENE-EXPRESSION; GROWTH-FACTOR; ANTIPROLIFERATIVE AGENTS; D1-DEPENDENT KINASE; DEPENDENT KINASES; PHASE PROGRESSION; NUCLEAR-PROTEIN
Publisher's Version: https://doi.org/10.1074/jbc.273.36.23104
Terms of Use/Rights Notice: Refer to copyright notice on published article.

Creation Date: 1998-09-04 12:00:00