Granulocyte macrophage colony-stimulating factor enhances retinoic acid-induced gene expression

2006 ◽  
Vol 80 (4) ◽  
pp. 889-896 ◽  
Author(s):  
Takahisa Shimizu ◽  
Lisa Esaki ◽  
Hiroko Mizuno ◽  
Ken Takeda
Keyword(s):  
Gene Expression ◽  
Retinoic Acid ◽  
Colony Stimulating Factor ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

scholarly journals Role of Granulocyte-Macrophage Colony-Stimulating Factor in Acute Myeloid Leukemia/Myelodysplastic Syndromes

2018 ◽  
pp. 1-6
Author(s):  
Neemat M. Kassem ◽  
Alya M. Ayad ◽  
Noha M. El Husseiny ◽  
Doaa M. El-Demerdash ◽  
Hebatallah A. Kassem ◽  
...  
Keyword(s):  
Gene Expression ◽  
Myeloid Leukemia ◽  
Serum Levels ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Acute Myeloid

Purpose Granulocyte-macrophage colony-stimulating factor (GM-CSF) cytokine stimulates growth, differentiation, and function of myeloid progenitors. We aimed to study the role of GM-CSF gene expression, its protein, and antibodies in patients with acute myeloid leukemia/myelodysplastic syndromes (AML/MDS) and their correlation to disease behavior and treatment outcome. The study included 50 Egyptian patients with AML/MDS in addition to 20 healthy volunteers as control subjects. Patients and Methods Assessment of GM-CSF gene expression was performed by quantitative real-time polymerase chain reaction. GM-CSF proteins and antibodies were assessed by enzyme-linked immunosorbent assay. Results There was significant decrease in GM-CSF gene expression ( P = .008), increase in serum level of GM-CSF protein ( P = .0001), and increase in anti–GM-CSF antibodies ( P = .001) in patients with AML/MDS compared with healthy control subjects. In addition, there was a significant negative correlation between serum levels of GM-CSF protein and initial peripheral blood blasts, percentage as well as response to therapy. Conclusion Any alteration in GM-CSF gene expression could have implications in leukemogenesis. In addition, GM-CSF protein serum levels could be used to predict outcome of therapy. GM-CSF antibodies may also play a role in the pathogenesis of AML/MDS. The use of these GM-CSF parameters for disease monitoring and as markers of disease activity needs further research.

scholarly journals STAT5A-Deficient Mice Demonstrate a Defect in Granulocyte-Macrophage Colony-Stimulating Factor–Induced Proliferation and Gene Expression

Blood ◽  
1997 ◽  
Vol 90 (5) ◽  
pp. 1768-1776 ◽  
Author(s):  
Gerald M. Feldman ◽  
Louis A. Rosenthal ◽  
Xiuwen Liu ◽  
Mark P. Hayes ◽  
Anthony Wynshaw-Boris ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Binding Proteins ◽  
Colony Stimulating Factor ◽  
Wild Type ◽  
Stat Proteins ◽  
Gm Csf ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
In Cells

Abstract Responses of cells to cytokines typically involve the activation of a family of latent DNA binding proteins, referred to as signal transducers and activators of transcription (STAT) proteins, which are critical for the expression of early response genes. Of the seven known STAT proteins, STAT5 (originally called mammary gland factor) has been shown to be activated by several cytokines, such as granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-3 (IL-3), and IL-5, which are known to play important roles in growth and differentiation of hematopoietic precursors. In this report we have used mice that are deficient in STAT5A (one of two homologues of STAT5) to study the role of STAT5A in GM-CSF stimulation of cells. When bone marrow–derived macrophages were generated by differentiation with macrophage-CSF (M-CSF), exposure of cells from wild-type mice to GM-CSF resulted in a typical pattern of assembly of DNA binding proteins specific for the gamma activation sequence (GAS) element within the β-casein promoter. However, in cells from the STAT5A null mouse one of the shifted bands was absent. Immunoblotting analysis in the null mice showed that lack of STAT5A protein resulted in no alteration in activation of STAT5B by tyrosine phosphorylation. Proliferation experiments revealed that, when exposed to increasing concentrations of GM-CSF, cells derived from the null mice grew considerably more slowly than cells derived from the wild-type mice. Moreover, expression of GM-CSF–dependent genes, CIS and A1, was markedly inhibited in cells derived from null mice as compared with those of wild-type mice. The decreased expression observed with A1, a bcl-2 like gene, may account in part for the suppression of growth in cells from the null mice. These data suggest that the presence of STAT5A during the GM-CSF–induced assembly of STAT5 dimers is critical for the formation of competent transcription factors that are required for both gene expression and cell proliferation.

The cytokines IL-3 and GM-CSF regulate the transcriptional activity of retinoic acid receptors in different in vitro models of myeloid differentiation

Blood ◽  
2002 ◽  
Vol 99 (3) ◽  
pp. 746-753 ◽  
Author(s):  
Barton S. Johnson ◽  
LeMoyne Mueller ◽  
Jutong Si ◽  
Steven J. Collins
Keyword(s):  
Retinoic Acid ◽  
Transcriptional Activity ◽  
In Vitro Models ◽  
Myeloid Differentiation ◽  
Colony Stimulating Factor ◽  
Interleukin 3 ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Abstract The disruption of retinoic acid receptor (RAR) activity that characterizes human acute promyelocytic leukemia (APL) is associated with a block to granulocytic differentiation indicating that RARs are critical regulators of normal myeloid differentiation. Nevertheless, how RAR activity might be regulated in the presumably homogenous concentration of retinoids in blood and bone marrow and how these receptors might interact with specific hematopoietic cytokines to regulate normal myeloid differentiation remain unclear. Here, using several cytokine-dependent in vitro models of myeloid development, it was observed that specific hematopoietic cytokines that normally regulate myeloid lineage commitment and differentiation (interleukin-3 and granulocyte-macrophage colony-stimulating factor) trigger the enhancement of both ligand-dependent and ligand-independent transcriptional activity of both endogenous and exogenous (transiently transfected) RARs. This cytokine-mediated enhancement of RAR activity is not associated with any observed changes in expression of the RARs or their respective coactivators/corepressors. These studies define a previously unknown cytokine-RAR interaction during myelopoiesis and suggest that RAR activation might be a critical downstream event following interleukin-3 and granulocyte-macrophage colony-stimulating factor signaling during myeloid differentiation. This observation of ligand-independent activation of RARs that is mediated by certain cytokines represents a new paradigm with respect to how RAR activity might be modulated during hematopoiesis and also suggests a molecular basis for the differential sensitivity of human acute myelogenous leukemia cells to retinoids.

Granulocyte-macrophage colony stimulating factor gene expression and function during tumor promotion

1994 ◽  
Vol 15 (5) ◽  
pp. 1017-1029 ◽  
Author(s):  
Fredika M. Robertson ◽  
Gautam N. Bijur ◽  
Andrew S. Oberyszyn ◽  
Arthur E. Pellegrini ◽  
Laszlo G. Boros ◽  
...  
Keyword(s):  
Gene Expression ◽  
Tumor Promotion ◽  
Colony Stimulating Factor ◽  
Factor Gene ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
And Function ◽  
Stimulating Factor

scholarly journals 125 CHANGES OF PLASMA MACROPHAGE COLONY-STIMULATING FACTOR LEVELS AND ITS GENE EXPRESSION IN PERIPHERAL WHITE BLOOD CELLS DURING PREGNANCY IN JAPANESE BLACK CATTLE

2005 ◽  
Vol 17 (2) ◽  
pp. 213
Author(s):  
K. Oshima ◽  
K. Yoshihara ◽  
H. Watanabe ◽  
T. Kojima ◽  
M. Komatsu ◽  
...  
Keyword(s):  
Gene Expression ◽  
White Blood Cells ◽  
Colony Stimulating Factor ◽  
Rt Pcr ◽  
Relative Level ◽  
Csf Levels ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Peripheral White Blood Cells ◽  
Stimulating Factor

Macrophage colony-stimulating factor (M-CSF) is a hemopoietic cytokine that plays a primary role in placental physiology. Gene expression of M-CSF in bovine intercaruncular endometrium shows an upward trend in mid-pregnancy. The objective of this study was to determine the plasma M-CSF levels and the M-CSF gene expression levels in maternal peripheral white blood cells (PWBCs) during pregnancy using ELISA and quantitative RT-PCR. In Experiment 1, the plasma M-CSF levels in 112 Japanese Black heifers or cows were determined. Animals were divided into four groups according to pregnancy stage: first- (n = 29), second- (n = 33), third- (n = 26) trimester, and non-pregnant (n = 24). ELISA for bovine M-CSF established by Yoshihara et al. (2003 Vet. Immunol. Immunopathol. 95, 103–111) was used according to their instructions. The absorbance was measured at 405 nm in the Biomek Plate Reader (Beckman Coulter, Fullerton, CA, USA). In Experiment 2, the plasma M-CSF levels and M-CSF gene expression levels in PWBCs during pregnancy were determined. The plasma samples for ELISA were obtained from 8 heifers and 3 cows every 1 and/or 2 weeks. The PWBCs samples for quantitative RT-PCR were obtained from 4 heifers every 1 and/or 4 weeks. All quantitative RT-PCR protocols were carried out according to the previous report (Oshima et al. 2003 Theriogenology 60, 1217–1226). The quantitative PCR assay used an ABI Prism 7700 Sequence Detector (Applied Biosystems, Foster City, CA, USA). Signals were detected according to the manufacturer's instructions. The relative level of M-CSF expression was calculated on the basis of glyceraldehyde-phosphate-dehydrogenase (GAPDH) quantity (in the method of calculation, the relative level = M-CSF quantity/GAPDH quantity). Data were analyzed by Kruskal-Wallis test. In Experiment 1, the plasma M-CSF level in second-trimester cows was significantly higher than those in other stages (P < 0.05). In Experiment 2, the plasma M-CSF levels were significantly higher in gestational age from −4 to 1 weeks compared with the last stage of pregnancy (P < 0.05). The levels decreased until 6 weeks, appeared to temporarily increase, and were relatively constant until 35 weeks. Macrophage colony-stimulating factor genes were expressed in all samples examined; the levels were relatively constant in early pregnancy, and then were widely varied until parturition. These results suggest that plasma M-CSF levels may be related to the maternal condition of pregnancy and to a slight extent to M-CSF gene expression in PWBCs. This work was supported in part by a Grant-in-aid from the Recombinant Cytokine Project (RCP2002-2110), provided by the Ministry of Agriculture, Forestry, and Fisheries, Japan.

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