PMID- 1338337
OWN - NLM
STAT- MEDLINE
DCOM- 19930419
LR  - 20171116
IS  - 0021-9541 (Print)
IS  - 0021-9541 (Linking)
VI  - 151
IP  - 3
DP  - 1992 Jun
TI  - Biochemical events accompanying macrophage activation and the inhibition of 
      colony-stimulating factor-1-induced macrophage proliferation by tumor necrosis 
      factor-alpha, interferon-gamma, and lipopolysaccharide.
PG  - 630-41
AB  - Agents that can arrest cellular proliferation are now providing insights into 
      mechanisms of growth factor action and how this action may be controlled. It is 
      shown here that the macrophage activating agents tumor necrosis factor-alpha (TNF 
      alpha), interferon-gamma (IFN gamma), and lipopolysaccharide (LPS) can maximally 
      inhibit colony stimulating factor-1 (CSF-1)-induced, murine bone marrow-derived 
      macrophage (BMM) DNA synthesis even when added 8-12 h after the growth factor, a 
      period coinciding with the G1/S-phase border of the BMM cell cycle. This 
      inhibition was independent of autocrine PGE2 production or increased cAMP levels. 
      In order to compare the mode of action of these agents, their effects on a number 
      of other BMM responses in the absence or presence of CSF-1 were examined. All 
      three agents stimulated BMM protein synthesis; TNF alpha and LPS, but not IFN 
      gamma, stimulated BMM Na+/H+ exchange and Na+,K(+)-ATPase activities, as well as 
      c-fos mRNA levels. IFN gamma did not inhibit the CSF-1-induced Na+,K(+)-ATPase 
      activity. TNF alpha and LPS inhibited both CSF-1-stimulated urokinase-type 
      plasminogen activator (u-PA) mRNA levels and u-PA activity in BMM, whereas IFN 
      gamma lowered only the u-PA activity. In contrast, LPS and IFN gamma, but not TNF 
      alpha, inhibited CSF-1-induced BMM c-myc mRNA levels, the lack of effect of TNF 
      alpha dissociating the inhibition of DNA synthesis and decreased c-myc mRNA 
      expression for this cytokine. These results indicate that certain biochemical 
      responses are common to both growth factors and inhibitors of BMM DNA synthesis 
      and that TNF alpha, IFN gamma, and LPS, even though they all have a common action 
      in suppressing DNA synthesis, activate multiple signaling pathways in BMM, only 
      some of which overlap or converge.
FAU - Vairo, G
AU  - Vairo G
AD  - Department of Medicine, University of Melbourne, Royal Melbourne Hospital, 
      Parkville, Victoria, Australia.
FAU - Royston, A K
AU  - Royston AK
FAU - Hamilton, J A
AU  - Hamilton JA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Carrier Proteins)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Proto-Oncogene Proteins c-fos)
RN  - 0 (Proto-Oncogene Proteins c-myc)
RN  - 0 (RNA, Messenger)
RN  - 0 (Sodium-Hydrogen Exchangers)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 81627-83-0 (Macrophage Colony-Stimulating Factor)
RN  - 82115-62-6 (Interferon-gamma)
RN  - 9007-49-2 (DNA)
RN  - E0399OZS9N (Cyclic AMP)
RN  - EC 3.4.21.73 (Urokinase-Type Plasminogen Activator)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Animals
MH  - Bone Marrow Cells
MH  - Carrier Proteins/metabolism
MH  - Cell Cycle
MH  - Cell Division
MH  - Cells, Cultured
MH  - Cyclic AMP/metabolism
MH  - DNA/biosynthesis/drug effects
MH  - Dinoprostone/metabolism
MH  - Interferon-gamma/pharmacology
MH  - Lipopolysaccharides/pharmacology
MH  - *Macrophage Activation
MH  - Macrophage Colony-Stimulating Factor/*antagonists & inhibitors/pharmacology
MH  - Macrophages/cytology/*immunology
MH  - Mice
MH  - Mice, Inbred C3H
MH  - Mice, Inbred CBA
MH  - Proto-Oncogene Proteins c-fos/metabolism
MH  - Proto-Oncogene Proteins c-myc/metabolism
MH  - RNA, Messenger/metabolism
MH  - Signal Transduction
MH  - Sodium-Hydrogen Exchangers
MH  - Tumor Necrosis Factor-alpha/*pharmacology
MH  - Urokinase-Type Plasminogen Activator/metabolism
EDAT- 1992/06/01 00:00
MHDA- 1992/06/01 00:01
CRDT- 1992/06/01 00:00
PHST- 1992/06/01 00:00 [pubmed]
PHST- 1992/06/01 00:01 [medline]
PHST- 1992/06/01 00:00 [entrez]
AID - 10.1002/jcp.1041510324 [doi]
PST - ppublish
SO  - J Cell Physiol. 1992 Jun;151(3):630-41. doi: 10.1002/jcp.1041510324.