PMID- 8981359
OWN - NLM
STAT- MEDLINE
DCOM- 19970410
LR  - 20091119
IS  - 1040-452X (Print)
IS  - 1040-452X (Linking)
VI  - 46
IP  - 1
DP  - 1997 Jan
TI  - CSF-1 and cell cycle control in macrophages.
PG  - 19-23
AB  - Control of cell proliferation involves a finely interwoven network of positive 
      and negative cell cycle regulators. Signal transduction pathways linking c-fms 
      (CSF-1R) to cellular proliferation and differentiation are being explored. Part 
      of the strategy is to use a series of G1 inhibitors to help pinpoint relevant 
      targets. Several inhibitors-8Br-cAMP, interferon gamma (IFN gamma), INF 
      alpha/beta, lipopolysaccharide (LPS), tumor necrosis factor-alpha (TNF alpha), 
      and dimethylamiloride-suppress CSF-1-stimulated proliferation in murine bone 
      marrow-derived macrophages (BMM) even when added in the mid- to late-G1 phase of 
      the cell cycle. The down-modulating effects of the inhibitors on the expression 
      of the following cell cycle regulators have been examined: c-myc, cyclin D1 and 
      D2, cdk4, Rb phosphorylation, E2F binding activity, ribonucleotide reductase 
      subunits, and PCNA. Some differences in the negative control of such regulators 
      were found, for example, in the manner in which IFN gamma and cAMP down-regulate 
      c-myc expression. Using blocking antibodies and BMM from type I IFN receptor 
      knockout mice, it appears that one of these inhibitors, IFN alpha/beta, acts as 
      an endogenous inhibitor in CSF-1-treated BMM and is also responsible, at least in 
      part, for the inhibition of cell cycle progression by LPS and TNF alpha. Another 
      strategy has been to attempt to relate early biochemical changes induced by CSF-1 
      to later changes in the G1 phase, partly by studying cycling versus noncycling 
      macrophages and partly by using cells expressing c-fms with tyrosine mutations in 
      the intracytoplasmic region. CSF-1-mediated effects on the following signal 
      transduction molecules in these systems will be described: PI3-kinase, myelin 
      basic protein kinases, Erks, and STAT transcription factors.
FAU - Hamilton, J A
AU  - Hamilton JA
AD  - University of Melbourne, Department of Medicine, Royal Melbourne Hospital, 
      Parkville, Victoria, Australia.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Mol Reprod Dev
JT  - Molecular reproduction and development
JID - 8903333
RN  - 0 (Interferon-alpha)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Nucleic Acid Synthesis Inhibitors)
RN  - 0 (Receptors, Interferon)
RN  - 0 (Retinoblastoma Protein)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 156986-95-7 (Receptor, Interferon alpha-beta)
RN  - 81627-83-0 (Macrophage Colony-Stimulating Factor)
RN  - EC 2.7.- (Protein Kinases)
SB  - IM
MH  - Animals
MH  - Bone Marrow Cells
MH  - Cell Cycle/drug effects/*physiology
MH  - Cell Division/drug effects
MH  - Interferon-alpha/physiology
MH  - Lipopolysaccharides/pharmacology
MH  - Macrophage Colony-Stimulating Factor/pharmacology/*physiology
MH  - Macrophages/*cytology/drug effects
MH  - Mice
MH  - Mice, Knockout
MH  - Nucleic Acid Synthesis Inhibitors/pharmacology
MH  - Phosphorylation
MH  - Protein Kinases/metabolism
MH  - Protein Processing, Post-Translational
MH  - Receptor, Interferon alpha-beta
MH  - Receptors, Interferon/deficiency/genetics
MH  - Retinoblastoma Protein/metabolism
MH  - Tumor Necrosis Factor-alpha/pharmacology
RF  - 13
EDAT- 1997/01/01 00:00
MHDA- 2000/06/20 09:00
CRDT- 1997/01/01 00:00
PHST- 1997/01/01 00:00 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1997/01/01 00:00 [entrez]
AID - 10.1002/(SICI)1098-2795(199701)46:1<19::AID-MRD4>3.0.CO;2-U [pii]
AID - 10.1002/(SICI)1098-2795(199701)46:1<19::AID-MRD4>3.0.CO;2-U [doi]
PST - ppublish
SO  - Mol Reprod Dev. 1997 Jan;46(1):19-23. doi: 
      10.1002/(SICI)1098-2795(199701)46:1<19::AID-MRD4>3.0.CO;2-U.