Mast cell growth factor (C-Kit Ligand) in combination with granulocyte-macrophage colony-stimulating factor and interleukin-3:in vivo hemopoietic effects in irradiated mice compared toin vitro effects

Biotherapy ◽  
1993 ◽  
Vol 7 (1) ◽  
pp. 13-26 ◽  
Author(s):  
M. L. Patchen ◽  
R. Fischer ◽  
T. J. MacVittie ◽  
F. R. Seiler ◽  
D. E. Williams
Keyword(s):  
Mast Cell ◽  
Growth Factor ◽  
Colony Stimulating Factor ◽  
Kit Ligand ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Factor C ◽  
Stimulating Factor ◽  
Mast Cell Growth Factor

scholarly journals Differentialin vivobiodistribution of131I-labeled exosomes from diverse cellular origins and its implication in the theranostic application

2019 ◽  
Author(s):  
Mohammad H. Rashid ◽  
Thaiz F. Borin ◽  
Roxan Ara ◽  
Kartik Angara ◽  
Jingwen Cai ◽  
...  
Keyword(s):  
Growth Factor ◽  
Interleukin 1 ◽  
Suppressor Cells ◽  
Vascular Endothelial ◽  
Colony Stimulating Factor ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Endothelial Growth Factor ◽  
Stimulating Factor

AbstractExosomes are critical mediators of intercellular crosstalk and regulator of cellular/tumor microenvironment. Exosomes have great prospects for clinical application as theranostic and prognostic probe. Nevertheless, the advancement of the exosomes research has been thwarted by limited knowledge elucidating the most efficient isolation method and theirin vivotrafficking. Here we have showed that combination of two size-based methods using 0.20 µm syringe filter and 100k centrifuge membrane filter followed by ultracentrifugation method yields a greater number of uniform exosomes. We also demonstrated the visual representation and quantification of differentialin vivodistribution of radioisotope131I-labelled exosomes from diverse cellular origins, e.g., tumor cells with or without treatments (HET0016 and GW2580), myeloid-derived suppressor cells and endothelial progenitor cells. We also determined that the distribution was dependent on the protein/cytokine contents of the exosomes. The appliedin vivoimaging modalities can be utilized to monitor disease progression, metastasis, and exosome-based targeted therapy.AbbreviationsbFGFbasic fibroblast growth factorCSF1Rcolony stimulating factor 1 receptorCTcomputed tomographyCTLA4cytotoxic T-lymphocyte-associated protein 4EGFepidermal growth factorEMTepithelial to mesenchymal transitionEVsextracellular vesiclesEPCsendothelial progenitor cellsFasLFas ligandG-CSFgranulocyte-colony stimulating factorGM-CSFgranulocyte-macrophage colony-stimulating factorHGFhepatocyte growth factorHSPheat shock proteinICAM-1intercellular adhesion molecule 1IFN-gammainterferon gammaIL – 1betainterleukin-1 betaIL – 1rainterleukin-1 receptor antagonistIL – 2interleukin-2IL – 4interleukin-4IL – 6interleukin-6IL – 7interleukin-7IL – 10interleukin-10IL – 12interleukin-12IL – 13interleukin-13IL – 17interleukin-17KCkeratinocyte-derived chemokineLIXlipopolysaccharide-induced CXC chemokineM-CSFmacrophage colony-stimulating factorMCP-1monocyte chemoattractant protein 1MDCmacrophage-derived chemokineMDSCsmyeloid derived suppressor cellsMFPmammary fat padMIP-1αmacrophage-inflammatory protein-1alphaMMP-2matrix metalloproteinase-2MRImagnetic resonance imagingNISsodium iodide symporterNTAnanoparticle tracking analysisPETpositron emission tomographyPF-4platelet factor 4RANTESregulated on activation, normal T cell expressed and secretedROIsregion of interestSDF-1αstromal cell-derived factor-1SEMstandard error of the meanSPECTsingle-photon emission computed tomographySCFstem cell factorTAMstumor-associated macrophagesTEMtransmission electron microscopyTIMP 2tissue inhibitors of metalloproteinases 2TLPCthin layer paper chromatographyTMEtumor microenvironmentTNF-αtumor necrosis factor-αTSLPthymic stromal lymphopoietinUCultracentrifugationVEGF-Avascular endothelial growth factor AVEGFR2vascular endothelial growth factor receptor 2.

In vivo effects of macrophage colony-stimulating factor on human monocyte function

1991 ◽  
Vol 77 (1) ◽  
pp. 25-31 ◽  
Author(s):  
Asim Khwaja ◽  
Beryl Johnson ◽  
Ian E. Addison ◽  
Kwee Yong ◽  
Karen Ruthven ◽  
...  
Keyword(s):  
Human Monocyte ◽  
Colony Stimulating Factor ◽  
Monocyte Function ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
In Vivo Effects ◽  
Stimulating Factor

Granulocyte-macrophage colony-stimulating factor (GM-CSF) increases plasma fibrinolytic activity in vivo

1994 ◽  
Vol 8 (1) ◽  
pp. 42-47 ◽  
Author(s):  
K.L. Yong ◽  
T. McNally ◽  
I.J. Mackie ◽  
H. Cohen ◽  
S.J. Machin ◽  
...  
Keyword(s):  
Fibrinolytic Activity ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

scholarly journals Enhanced survival but reduced engraftment in murine recipients of recombinant granulocyte/macrophage colony-stimulating factor following transplantation of T-cell-depleted histoincompatible bone marrow

Blood ◽  
1988 ◽  
Vol 72 (4) ◽  
pp. 1148-1154 ◽  
Author(s):  
BR Blazar ◽  
MB Widmer ◽  
CC Soderling ◽  
S Gillis ◽  
DA Vallera
Keyword(s):  
Bone Marrow ◽  
T Cell ◽  
Hematological Parameters ◽  
Donor Cell ◽  
Colony Stimulating Factor ◽  
Murine Bone Marrow ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Abstract In vivo administration of murine recombinant granulocyte/macrophage colony stimulating factor (rGM-CSF) was evaluated for effects on survival and engraftment in an allogeneic murine bone marrow transplantation (BMT) model involving T-cell depletion of donor marrow. The model provides a high incidence of graft failure/rejection. Recipients of continuous subcutaneous infusions of rGM-CSF had a significant survival advantage when compared with untreated controls. However, a significantly lower incidence of donor cell engraftment was noted. Hematological parameters were not substantially affected. When rGM-CSF was administered intraperitoneally (IP), twice daily injections closely approximated the effects of continuous infusion on survival. Single IP injections were without significant effects on survival or engraftment. These results demonstrate that prolonged frequent in vivo exposure to rGM-CSF can significantly improve survival but significantly decreases donor cell repopulation in recipients of T-cell- depleted histoincompatible marrow grafts.

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.

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