Messenger RNA Expression of Granulocyte Colony-Stimulating Factor Receptor Isoforms in the Fetus

2003 ◽  
Vol 83 (3) ◽  
pp. 191-196 ◽  
Author(s):  
Jason A. Gersting ◽  
Yan Du ◽  
Robert D. Christensen ◽  
Darlene A. Calhoun
Keyword(s):  
Messenger Rna ◽  
Rna Expression ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Receptor Isoforms ◽  
Stimulating Factor

Autocrine production of epithelial cell–derived neutrophil attractant-78 induced by granulocyte colony-stimulating factor in neutrophils

Blood ◽  
2002 ◽  
Vol 99 (5) ◽  
pp. 1863-1865 ◽  
Author(s):  
Sachiko Suzuki ◽  
Masanobu Kobayashi ◽  
Kouji Chiba ◽  
Iori Horiuchi ◽  
Jingxin Wang ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Dna Microarray ◽  
Messenger Rna ◽  
Chemotactic Factor ◽  
Rna Expression ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Dna Microarray System ◽  
Stimulating Factor ◽  
Factor G

Whereas mobilization to inflammatory sites is an important function of neutrophils, it remains to be determined whether granulocyte colony-stimulating factor (G-CSF) stimulates the mobilization of neutrophils to the inflammatory sites. This study compared the expression of more than 9000 genes in neutrophils treated with and without G-CSF with the use of a DNA microarray system to determine the effects of G-CSF on the function of neutrophils. It was found that messenger RNA expression of epithelial cell–derived neutrophil attractant-78 (ENA-78), which has been reported to be a chemotactic factor for neutrophils, was induced by G-CSF in neutrophils. The study demonstrated that the supernatant of G-CSF–treated neutrophils induced the chemotaxis of neutrophils and that anti–ENA-78 antibody and anti–CXCR-2 antibody inhibited the chemotaxis. These data suggest that G-CSF may enhance the mobilization of neutrophils and consequently augment the accumulation of neutrophils in the inflammatory sites through the secretion of ENA-78.

scholarly journals Granulocyte colony-stimulating factor stimulates human mature neutrophilic granulocytes to produce interferon-alpha

Blood ◽  
1990 ◽  
Vol 75 (1) ◽  
pp. 17-19 ◽  
Author(s):  
N Shirafuji ◽  
S Matsuda ◽  
H Ogura ◽  
K Tani ◽  
H Kodo ◽  
...  
Keyword(s):  
Interferon Alpha ◽  
Messenger Rna ◽  
Mononuclear Cells ◽  
Human Neutrophils ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Glycoprotein Hormone ◽  
Ifn Alpha ◽  
Stimulating Factor

Abstract Granulocyte colony-stimulating factor (G-CSF) is a glycoprotein hormone that specifically stimulates both production and functional activation of neutrophils, while interferon-alpha (IFN-alpha) is known to suppress myelopoiesis, including neutrophil production in vivo and in vitro. On a possibility that IFN-alpha may operate as one of the inhibitory feedback factors in neutropoiesis, we examined whether neutrophils produce IFN-alpha in response to G-CSF. Northern blot analysis showed that messenger RNA (mRNA) for human IFN-alpha 1 became detectable time- dependently in highly purified human neutrophils incubated with purified recombinant human G-CSF (rhG-CSF). But such transcription was not observed either in neutrophils incubated with other neutrophil activators, such as formyl-methionyl-leucyl-phenylalanine (fMLP) or lipopolysaccharides (LPS), or in blood mononuclear cells incubated with rhG-CSF. In addition, radioimmunoassay for human IFN-alpha showed that its levels in culture medium of the rhG-CSF-treated neutrophils rose markedly (up to approximately 100 IU/mL/1 x 10(7) cells) in a time- dependent way, compared with those of nonstimulated neutrophils. These findings suggest that the G-CSF/IFN-alpha system may participate in the feedback regulatory loop of neutropoiesis.

Time course of increasing numbers of mutations in the granulocyte colony-stimulating factor receptor gene in a patient with congenital neutropenia who developed leukemia

Blood ◽  
2001 ◽  
Vol 97 (6) ◽  
pp. 1882-1884 ◽  
Author(s):  
Christoph A. Tschan ◽  
Christina Pilz ◽  
Cornelia Zeidler ◽  
Karl Welte ◽  
Manuela Germeshausen
Keyword(s):  
Messenger Rna ◽  
Time Course ◽  
Mononuclear Cells ◽  
Receptor Gene ◽  
Point Mutations ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Congenital Neutropenia ◽  
Polymerase Chain ◽  
Stimulating Factor

Point mutations in the granulocyte colony-stimulating factor receptor (G-CSFR) gene have been linked to the development of secondary leukemia in patients with congenital neutropenia (CN). This report presents data on a now 18-year-old patient with CN who has received G-CSF treatment since 1989 and who developed acute myeloid leukemia (AML) in 1998. To evaluate whether there is an association between the occurrence of point mutations of the G-CSFR gene and development of secondary AML, DNA/messenger RNA of neutrophils and mononuclear cells from this patient were analyzed at different time points by polymerase chain reaction and subsequent cloning by DNA sequencing of representative numbers of individual clones. Findings suggest an increasing instability of the G-CSFR gene in time as judged by increasing numbers of mutations proposed to be one important step in the development of AML in this patient.

Granulocyte Colony-Stimulating Factor–Producing Undifferentiated Sarcoma Occurring in Previously Fractured Femur

2003 ◽  
Vol 127 (4) ◽  
pp. e186-e189
Author(s):  
Takashi Marui ◽  
Tetsuji Yamamoto ◽  
Toshihiro Akisue ◽  
Toshiaki Hitora ◽  
Shinichi Yoshiya ◽  
...  
Keyword(s):  
Messenger Rna ◽  
Culture Medium ◽  
Soft Tissue Tumor ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Undifferentiated Sarcoma ◽  
Genomic Study ◽  
Polymerase Chain ◽  
Stimulating Factor

Abstract We examined the case of a 52-year-old man presenting with a sarcoma accompanied by severe leukocytosis, which developed many years after a femoral fracture. Histologic, histochemical, immunohistochemical, and ultrastructural analysis of the tumor revealed that the sarcoma could not be classified by any of the bone or soft tissue tumor classifications currently in use. The tumor cells were isolated from surgical specimens and subcultured in vitro. The concentration of granulocyte colony-stimulating factor in the culture medium was constantly elevated to considerably high levels during 20 cell passages. A genomic study using reverse transcription–polymerase chain reaction showed that the cells retained messenger RNA expression of granulocyte colony-stimulating factor. The aberrant overexpression of granulocyte colony-stimulating factor clearly represented a paraneoplastic phenomenon of the neoplastic cells.

Cyclophosphamide/granulocyte colony-stimulating factor causes selective mobilization of bone marrow hematopoietic stem cells into the blood after M phase of the cell cycle

Blood ◽  
2001 ◽  
Vol 97 (8) ◽  
pp. 2278-2285 ◽  
Author(s):  
Douglas E. Wright ◽  
Samuel H. Cheshier ◽  
Amy J. Wagers ◽  
Troy D. Randall ◽  
Julie L. Christensen ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Bone Marrow ◽  
Hematopoietic Stem Cells ◽  
Messenger Rna ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Hematopoietic Stem ◽  
M Phase ◽  
Stimulating Factor

Abstract Cytokine-mobilized peripheral blood hematopoietic stem cells (MPB HSC) are widely used for transplantation in the treatment of malignancies, but the mechanism of HSC mobilization is unclear. Although many HSC in bone marrow (BM) cycle rapidly and expand their numbers in response to cytoreductive agents, such as cyclophosphamide (CY), and cytokines, such as granulocyte colony-stimulating factor (G-CSF), MPB HSC are almost all in the G0 or G1phase of the cell cycle. This has raised the question of whether a subset of noncycling BM HSC is selectively released, or whether cycling BM HSC are mobilized after M phase, but before the next S phase of the cell cycle. To distinguish between these possibilities, mice were treated with one dose of CY followed by daily doses of G-CSF, and dividing cells were marked by administration of bromodeoxyuridine (BrdU) during the interval that BM HSC are expanding. After CY and 4 days of G-CSF, 98.5% of the 2n DNA content long-term repopulating MPB (LT)-HSC stained positively for BrdU, and therefore derived from cells that divided during the treatment interval. Next, LT-HSC from mice previously treated with a single dose of CY, which kills cycling cells, and 3 daily doses of G-CSF, were nearly all killed by a second dose of CY, suggesting that CY/G-CSF causes virtually all LT-HSC to cycle. Analysis of cyclin D2 messenger RNA (mRNA) expression and total RNA content of MPB HSC suggests that these cells are mostly in G1 phase. After CY/G-CSF treatment, virtually all BM LT-HSC enter the cell cycle; some of these HSC then migrate into the blood, specifically after M phase, and are rapidly recruited to particular hematopoietic organs.

scholarly journals Granulocyte colony-stimulating factor stimulates human mature neutrophilic granulocytes to produce interferon-alpha

Blood ◽  
1990 ◽  
Vol 75 (1) ◽  
pp. 17-19 ◽  
Author(s):  
N Shirafuji ◽  
S Matsuda ◽  
H Ogura ◽  
K Tani ◽  
H Kodo ◽  
...  
Keyword(s):  
Interferon Alpha ◽  
Messenger Rna ◽  
Mononuclear Cells ◽  
Human Neutrophils ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Glycoprotein Hormone ◽  
Ifn Alpha ◽  
Stimulating Factor

Granulocyte colony-stimulating factor (G-CSF) is a glycoprotein hormone that specifically stimulates both production and functional activation of neutrophils, while interferon-alpha (IFN-alpha) is known to suppress myelopoiesis, including neutrophil production in vivo and in vitro. On a possibility that IFN-alpha may operate as one of the inhibitory feedback factors in neutropoiesis, we examined whether neutrophils produce IFN-alpha in response to G-CSF. Northern blot analysis showed that messenger RNA (mRNA) for human IFN-alpha 1 became detectable time- dependently in highly purified human neutrophils incubated with purified recombinant human G-CSF (rhG-CSF). But such transcription was not observed either in neutrophils incubated with other neutrophil activators, such as formyl-methionyl-leucyl-phenylalanine (fMLP) or lipopolysaccharides (LPS), or in blood mononuclear cells incubated with rhG-CSF. In addition, radioimmunoassay for human IFN-alpha showed that its levels in culture medium of the rhG-CSF-treated neutrophils rose markedly (up to approximately 100 IU/mL/1 x 10(7) cells) in a time- dependent way, compared with those of nonstimulated neutrophils. These findings suggest that the G-CSF/IFN-alpha system may participate in the feedback regulatory loop of neutropoiesis.

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