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Autocrine regulation of macrophage proliferation by tumor necrosis factor-alpha.
Exp Hematol. 1996 May; 24(6):675-81.EH

Abstract

We have examined production of tumor necrosis factor-alpha (TNF-alpha) from mouse bone marrow-derived macrophages (BMM) after stimulation by lipopolysaccharide (LPS), macrophage colony-stimulating factor (M-CSF/CSF-1), or granulocyte-macrophage colony-stimulating factor (GM-CSF). To control for effects of trace levels of LPS in culture media, we examined CSF-1 and GM-CSF-stimulated TNF-alpha production in relatively homogeneous populations of normal LPS-hyporesponsive C3H/HeJ BMM and a growth factor-dependent cell line (S1) of C3H/HeJ origin. We found that both TNF-alpha mRNA and protein are induced in these macrophage populations by CSF-1 stimulation alone. Stimulation with GM-CSF, however, appears to negatively regulate TNF-alpha protein levels. Most TNF-alpha detectable after CSF-1 or GM-CSF stimulation was cell associated. Only stimulation by LPS resulted in large amounts of released TNF-alpha detectable in culture supernatant. The hypothesis that endogenously produced TNF-alpha can function as an autocrine growth factor for CSF-1-stimulated proliferation was supported by the demonstration of a partial inhibition of BMM proliferation (p < 0.05) in the presence of a neutralizing anti-TNF-alpha antiserum. These results demonstrate that CSF-1 alone is capable of inducing expression of both TNF-alpha mRNA and protein, that GM-CSF may negatively regulate TNF-alpha protein production, and that endogenously produced TNF-alpha may provide additional growth signals for CSF-1 mediated BMM proliferation.

Authors+Show Affiliations

Canadian Red Cross Blood Transfusion Centre, Edmonton, Alberta, Canada.No affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

8635522

Citation

Branch, D R., and L J. Guilbert. "Autocrine Regulation of Macrophage Proliferation By Tumor Necrosis Factor-alpha." Experimental Hematology, vol. 24, no. 6, 1996, pp. 675-81.
Branch DR, Guilbert LJ. Autocrine regulation of macrophage proliferation by tumor necrosis factor-alpha. Exp Hematol. 1996;24(6):675-81.
Branch, D. R., & Guilbert, L. J. (1996). Autocrine regulation of macrophage proliferation by tumor necrosis factor-alpha. Experimental Hematology, 24(6), 675-81.
Branch DR, Guilbert LJ. Autocrine Regulation of Macrophage Proliferation By Tumor Necrosis Factor-alpha. Exp Hematol. 1996;24(6):675-81. PubMed PMID: 8635522.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Autocrine regulation of macrophage proliferation by tumor necrosis factor-alpha. AU - Branch,D R, AU - Guilbert,L J, PY - 1996/5/1/pubmed PY - 1996/5/1/medline PY - 1996/5/1/entrez SP - 675 EP - 81 JF - Experimental hematology JO - Exp Hematol VL - 24 IS - 6 N2 - We have examined production of tumor necrosis factor-alpha (TNF-alpha) from mouse bone marrow-derived macrophages (BMM) after stimulation by lipopolysaccharide (LPS), macrophage colony-stimulating factor (M-CSF/CSF-1), or granulocyte-macrophage colony-stimulating factor (GM-CSF). To control for effects of trace levels of LPS in culture media, we examined CSF-1 and GM-CSF-stimulated TNF-alpha production in relatively homogeneous populations of normal LPS-hyporesponsive C3H/HeJ BMM and a growth factor-dependent cell line (S1) of C3H/HeJ origin. We found that both TNF-alpha mRNA and protein are induced in these macrophage populations by CSF-1 stimulation alone. Stimulation with GM-CSF, however, appears to negatively regulate TNF-alpha protein levels. Most TNF-alpha detectable after CSF-1 or GM-CSF stimulation was cell associated. Only stimulation by LPS resulted in large amounts of released TNF-alpha detectable in culture supernatant. The hypothesis that endogenously produced TNF-alpha can function as an autocrine growth factor for CSF-1-stimulated proliferation was supported by the demonstration of a partial inhibition of BMM proliferation (p < 0.05) in the presence of a neutralizing anti-TNF-alpha antiserum. These results demonstrate that CSF-1 alone is capable of inducing expression of both TNF-alpha mRNA and protein, that GM-CSF may negatively regulate TNF-alpha protein production, and that endogenously produced TNF-alpha may provide additional growth signals for CSF-1 mediated BMM proliferation. SN - 0301-472X UR - https://www.unboundmedicine.com/medline/citation/8635522/Autocrine_regulation_of_macrophage_proliferation_by_tumor_necrosis_factor_alpha_ L2 - https://antibodies.cancer.gov/detail/CPTC-CSF1-1 DB - PRIME DP - Unbound Medicine ER -