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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.
J Cell Physiol. 1992 Jun; 151(3):630-41.JC

Abstract

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.

Authors+Show Affiliations

Department of Medicine, University of Melbourne, Royal Melbourne Hospital, Parkville, Victoria, Australia.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

1338337

Citation

Vairo, G, et al. "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." Journal of Cellular Physiology, vol. 151, no. 3, 1992, pp. 630-41.
Vairo G, Royston AK, Hamilton JA. 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. J Cell Physiol. 1992;151(3):630-41.
Vairo, G., Royston, A. K., & Hamilton, J. A. (1992). 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. Journal of Cellular Physiology, 151(3), 630-41.
Vairo G, Royston AK, Hamilton JA. 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. J Cell Physiol. 1992;151(3):630-41. PubMed PMID: 1338337.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 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. AU - Vairo,G, AU - Royston,A K, AU - Hamilton,J A, PY - 1992/6/1/pubmed PY - 1992/6/1/medline PY - 1992/6/1/entrez SP - 630 EP - 41 JF - Journal of cellular physiology JO - J Cell Physiol VL - 151 IS - 3 N2 - 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. SN - 0021-9541 UR - https://www.unboundmedicine.com/medline/citation/1338337/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_ L2 - https://doi.org/10.1002/jcp.1041510324 DB - PRIME DP - Unbound Medicine ER -