Macrophage Colony-Stimulating Factor Accelerates Wound Healing and Upregulates TGF-β1 mRNA Levels through Tissue Macrophages

1997 ◽  
Vol 72 (2) ◽  
pp. 162-169 ◽  
Author(s):  
Liancun Wu ◽  
Yung L. Yu ◽  
Robert D. Galiano ◽  
Sanford I. Roth ◽  
Thomas A. Mustoe
Keyword(s):  
Wound Healing ◽  
Mrna Levels ◽  
Colony Stimulating Factor ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Tgf Β1

Regulation of macrophage colony-stimulating factor in liver fat-storing cells by peptide growth factors

1992 ◽  
Vol 262 (4) ◽  
pp. C876-C881 ◽  
Author(s):  
M. Pinzani ◽  
H. E. Abboud ◽  
L. Gesualdo ◽  
S. L. Abboud
Keyword(s):  
Growth Factor ◽  
Constitutive Expression ◽  
Liver Fat ◽  
Northern Analysis ◽  
Mrna Levels ◽  
Colony Stimulating Factor ◽  
Term Survival ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Macrophage colony-stimulating factor (M-CSF) selectively promotes mononuclear phagocyte survival, proliferation, and differentiation. The production of this factor within the liver may be necessary to support the relatively long-term survival of circulating monocytes as they migrate into tissues and differentiate into macrophages. We studied the constitutive expression and the effects of platelet-derived growth factor (PDGF), basic fibroblast growth factor (bFGF), and epidermal growth factor (EGF) on M-CSF mRNA levels and secretion of M-CSF in murine liver fat-storing cells (FSC), vascular pericytes likely involved in the development of liver fibrosis. By Northern analysis, using a murine M-CSF cDNA, FSC constitutively express two major transcripts of 4.4 and 2.2 kb, similar to those detected in mouse L cells, used as a control. Exposure to 10 ng/ml PDGF or bFGF increased M-CSF mRNA levels. Peak effects were observed at 3 and 6 h for PDGF and bFGF, respectively, returning to baseline levels by 12 h. Under basal conditions, detectable amounts of M-CSF, measured by radioimmunoassay, were found in cell supernatants conditioned for 8 and 24 h. PDGF and bFGF markedly stimulated the release of M-CSF as early as 8 h, an effect persisting for at least 24 h. These findings suggest that liver FSC release M-CSF upon stimulation by PDGF and bFGF and may contribute to the activation of resident or infiltrating cells in inflammatory liver diseases.

Inhibitor of nuclear factor-κB induction by cAMP antagonizes interleukin-1-induced human macrophage-colony-stimulating-factor expression

2001 ◽  
Vol 356 (2) ◽  
pp. 525-530 ◽  
Author(s):  
Pisate J. KAMTHONG ◽  
Ming-chi WU
Keyword(s):  
Nuclear Factor Κb ◽  
Human Macrophage ◽  
Mrna Levels ◽  
Nuclear Factor ◽  
Colony Stimulating Factor ◽  
Dibutyryl Camp ◽  
Iκb Kinase ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

We have recently reported that interleukin-1α (IL-1α) can induce human macrophage colony-stimulating factor (M-CSF) expression through nuclear factor κB (NF-κB) activation, and treatment of human pancreatic MIA PaCa-2 cancer cells with forskolin or cAMP attenuated the NF-κB activation as well as M-CSF expression. In this study, we have further investigated the mechanism of cAMP attenuation. MIA PaCa-2 cells were incubated with forskolin or dibutyryl-cAMP and then stimulated with IL-1 for 1h. Cell lysates were immunoprecipitated by anti-inhibitory κB (IκB) kinase-β (IKKβ) antibody and the immune complex assayed for kinase activity using recombinant inhibitor of NF-κB (IκBα) as substrate. The levels of IKKβ in the respective cellular proteins were measured by subsequent Western blot. The results show that the level of IKK protein remains constant in the presence of cAMP, forskolin and/or IL-1, whereas IKK activity was robustly stimulated by IL-1. Nonetheless, dibutyryl-cAMP or forskolin did not affect the IKK activation induced by IL-1. This experiment suggests that elevated cAMP has no effect on IKK activity. IκBα protein level decreased markedly in IL-1-treated cells compared with the untreated. By contrast, cells treated with cAMP or forskolin possessed discernibly higher IκBα levels. In addition, we observed that forskolin potentiated and prolonged the IL-1-induced IκBα mRNA levels, whereas it did not stabilize the IκBα mRNA message. Wholly, these studies indicate that elevated cAMP antagonizes IL-1-induced M-CSF transcription by up-regulating IκBα gene induction and its consequent attenuation of NF-κB activation.

scholarly journals Macrophage colony-stimulating factor and granulocyte-macrophage colony- stimulating factor stimulate the synthesis of plasminogen-activator inhibitors by human monocytes

Blood ◽  
1993 ◽  
Vol 82 (12) ◽  
pp. 3616-3621 ◽  
Author(s):  
JA Hamilton ◽  
GA Whitty ◽  
H Stanton ◽  
J Wojta ◽  
M Gallichio ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Human Monocyte ◽  
Mrna Levels ◽  
Human Monocytes ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Pai 1

Macrophage colony-stimulating factor (M-CSF or CSF-1) and granulocyte- macrophage CSF (GM-CSF) have been shown to increase human monocyte urokinase-type plasminogen-activator (u-PA) activity with possible consequences for cell migration and tissue remodeling; because monocyte u-PA activity is likely to be controlled in part also by the PA inhibitors (PAIs) made by the cell, the effect of M-CSF and GM-CSF on human monocyte PAI-2 and PAI-1 synthesis was investigated. To this end, elutriation-purified human monocytes were treated in vitro with purified recombinant human M-CSF and GM-CSF, and PAI-2 and PAI-1 antigen and mRNA levels measured by specific enzyme-linked immunosorbent assays and Northern blot, respectively. Each CSF could enhance the protein and mRNA levels of PAI-2 and PAI-1 at similar concentrations for each product. This similar regulation of monocyte PAI expression in response to the CSFs contrasted with that found for the effects of lipopolysaccharide, transforming growth factor-beta and a glucocorticoid. Therefore, PAIs may be modulating the effects of the CSFs on monocyte u-PA activity at sites of inflammation and tissue remodeling.

Local Granulocyte-Macrophage Colony-Stimulating Factor Improves Incisional Wound Healing in Adriamycin-Treated Rats

Surgery Today ◽  
2005 ◽  
Vol 36 (1) ◽  
pp. 47-51 ◽  
Author(s):  
Mehmet Ali Gulcelik ◽  
Soykan Dinc ◽  
Meral Dinc ◽  
Erdinc Yenidogan ◽  
Huseyın Ustun ◽  
...  
Keyword(s):  
Wound Healing ◽  
Colony Stimulating Factor ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Bcl-3 Expression and Nuclear Translocation Are Induced by Granulocyte-Macrophage Colony-Stimulating Factor and Erythropoietin in Proliferating Human Erythroid Precursors

Blood ◽  
1998 ◽  
Vol 92 (4) ◽  
pp. 1225-1234 ◽  
Author(s):  
Min-Ying Zhang ◽  
Edward W. Harhaj ◽  
Laurie Bell ◽  
Shao-Cong Sun ◽  
Barbara A. Miller
Keyword(s):  
Nuclear Translocation ◽  
Mrna Levels ◽  
Colony Stimulating Factor ◽  
Reporter Plasmid ◽  
Gm Csf ◽  
Erythroid Precursors ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Stimulation Of

Bcl-3 is a proto-oncogene involved in the chromosomal translocation t(14;19) found in some patients with chronic lymphocytic leukemia. It shares structural similarities with and is a member of the IκB family of proteins. In this report, involvement of Bcl-3in hematopoietic growth factor-stimulated erythroid proliferation and differentiation was examined. In TF-1 cells, an erythroleukemia cell line, granulocyte-macrophage colony-stimulating factor (GM-CSF) and erythropoietin (Epo) greatly enhanced Bcl-3 expression at both the protein and mRNA levels in association with stimulation of proliferation. Bcl-3 protein was also highly expressed in early burst-forming unit-erythroid (BFU-E)–derived erythroid precursors (day 7) and decreased during maturation (days 10 and 14), suggesting that Bcl-3 is involved in normal erythroid proliferation. In these hematopoietic cells, Bcl-3 was hyperphosphorylated. GM-CSF and Epo modulated the subcellular localization of Bcl-3. Upon stimulation of TF-1 cells with GM-CSF or Epo, the nuclear translocation ofBcl-3 was dramatically enhanced. Overexpression of Bcl-3 in TF-1 cells by transient transfection along with the NF-κB factors p50 or p52 resulted in significant induction of an human immunodeficiency virus–type 1 (HIV-1) κB-TATA-luceriferase reporter plasmid, demonstrating that Bcl-3 has a positive role in transactivation of κB-containing genes in erythroid cells. Stimulation with GM-CSF enhanced c-myb mRNA expression in these cells. Bcl-3 in nuclear extracts of TF-1 cells bound to a κB enhancer in the c-mybpromoter together with NF-κB2/p52 and this binding activity was enhanced by GM-CSF stimulation. Furthermore, cotransfection of Bcl-3 with p52 or p50 in TF-1 cells resulted in significant activation of ac-myb κB-TATA-luceriferase reporter plasmid. These findings suggest that Bcl-3 may participate in the transcriptional regulation of certain κB-containing genes involved in hematopoiesis, includingc-myb. © 1998 by The American Society of Hematology.

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