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Colony-stimulating Factor Receptor (colony-stimulating + factor_receptor)

Distribution by Scientific Domains
Medical Sciences83%

Kinds of Colony-stimulating Factor Receptor

  • granulocyte colony-stimulating factor receptor
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    Selected Abstracts

    Comparative analysis of G-CSFR and GM-CSFR expressions on CD34+ cells in patients with aplastic anemia and myelodysplastic syndrome

    INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 6 2009
    H. XU
    Summary The aim of this article was to explore the pathogenetic differences, as well as to provide a new way for the differential diagnosis of these two diseases by comparative analysis of CD34+ cells numbers and their surface expression of granulocyte colony-stimulating factor receptor (G-CSFR) and granulocyte-macrophage colony-stimulating factor receptor (GM-CSFR) in patients with aplastic anemia (AA) and myelodysplastic syndrome (MDS). Twenty-seven patients with AA, 45 patients with MDS, and 20 normal controls were enrolled in this study. The ratio of CD34+ cells and their surface expression of G-CSFR and GM-CSFR were detected by flow cytometry (FCM). The ratio of CD34+ cells in BMMNC of AA, MDS patients and controls were 0.2438 ± 0.1129%, 2.1677 ± 1.1345% and 1.0792 ± 0.3221%, respectively. Compared with normal controls as well as MDS patients, the ratio of CD34+ cells in BMMNC of AA was significantly reduced (P < 0.05). The ratio of CD34+ cells in MDS was significantly elevated than controls (P < 0.05). The ratio of CD34+ cells in BMMNC of MDS-RA and MDS-RAEB patients were 1.2821 ± 0.4658% and 3.7729 ± 2.3360%, respectively. Compared with normal controls and MDS-RA patients, the ratio of CD34+ cells in MDS-RAEB was significantly elevated (P < 0.05). The ratio of CD34+ cells in MDS-RA was significantly elevated than AA patients (P < 0.05). The surface expression of G-CSFR on CD34+ cells of AA, MDS patients and controls were 34.402 ± 21.8357%, 26.376 ± 15.2895% and 21.443 ± 7.4465%, respectively. The surface expression of G-CSFR on CD34+ cells of MDS-RA and MDS-RAEB patients were 22.788 ± 14.7628% and 30.682 ± 15.5346%. The surface expression of GM-CSFR on CD34+ cells of AA, MDS patients and controls were 6.5961 ± 4.4322%, 18.2737 ± 10.9841% and 4.2753 ± 2.6249%, respectively. Compared with AA and controls, the expression of GM-CSFR in MDS patients was significantly elevated (P < 0.05). The surface expression of GM-CSFR on CD34+ cells of MDS-RA and MDS-RAEB patients were 16.1625 ± 6.9487% and 22.1003 ± 14.2983%. In AA patients, the ratio of CD34+ cells in BMMNC less than 0.1% accounts for 75% (6/8) SAA patients, compared with 10.55% (2/19) in CAA (P < 0.05). The detection of CD34+ cells and their surface expression of granulocyte (macrophage) colony-stimulating factor receptors G (M)-CSFR in AA and MDS are helpful in the differential diagnosis or prognosis of these two disorders. [source]

    Proteolytic cleavage of granulocyte colony-stimulating factor and its receptor by neutrophil elastase induces growth inhibition and decreased cell surface expression of the granulocyte colony-stimulating factor receptor

    AMERICAN JOURNAL OF HEMATOLOGY, Issue 3 2003
    Melissa G. Hunter
    Abstract Neutrophil elastase (NE) is a serine protease stored in the primary granules of neutrophils that proteolytically cleaves multiple cytokines and cell surface proteins on release from activated neutrophils. Recent reports of mutations in the gene encoding this enzyme in some patients with neutropenic syndromes prompted us to investigate whether granulocyte colony-stimulating factor (G-CSF) and its receptor (G-CSFR) are also substrates for NE. To further address this, we examined the effect of NE on G-CSF and the G-CSFR both in solution and on intact cells. Incubation of recombinant G-CSF or a G-CSFR form corresponding to its extracellular domain with purified NE resulted in rapid proteolytic cleavage of both proteins. Addition of NE to tissue culture medium or pretreatment of G-CSF with NE before its addition to media suppressed the growth of G-CSF,responsive cells. NE also cleaved the G-CSFR on the surface of intact cells resulting in a time-dependent reduction in cell surface expression of the G-CSFR. Notably, decreased G-CSFR surface expression resulting from treatment of cells with NE was also associated with a reduction in cell viability and proliferation in response to G-CSF. These results are the first to demonstrate that G-CSF and G-CSFR are proteolytically cleaved by NE and that NE-induced degradation of these proteins correlates with a reduction in the biologic activity of the cytokine and a decrease in the signaling function of the receptor because of decreased G-CSFR surface expression. These findings provide additional insights into mechanisms by which G-CSF/G-CSFR interactions may be modulated. Am. J. Hematol. 74:149,155, 2003. © 2003 Wiley-Liss, Inc. [source]

    In vivo expansion of transduced murine hematopoietic cells with a selective amplifier gene

    THE JOURNAL OF GENE MEDICINE, Issue 3 2003
    Akihiro Kume
    Abstract Background Hematopoietic stem-cell-directed gene transfer has achieved limited success in transducing clinically relevant levels of target cells. The expansion of gene-modified cells is one way to circumvent the problem of inefficient transduction with current vectors. To this end, we have developed ,selective amplifier genes' (SAGs) that encode chimeric proteins that are a fusion of granulocyte colony-stimulating factor receptor and the steroid-binding domain. Prototype SAGs conferred estrogen-responsive growth on murine hematopoietic progenitors. Methods We constructed a retroviral vector coexpressing an SAG for 4-hydroxytamoxifen (Tm)-specific proliferation and the enhanced green fluorescent protein (EGFP). Murine bone marrow cells were transduced with this vector and transplanted into myeloablated mice. Subsequently, recipients were challenged with Tm, and EGFP+ cells were enumerated. Results The challenge induced a significant increase in EGFP+ leukocytes (21 ± 4% to 27 ± 5%), while EGFP+ cells decreased in untreated animals (21 ± 5% to 10 ± 3%). Three months later, bone marrow cells were transplanted from the unchallenged mice to secondary hosts. Again the administration of Tm resulted in an increase of EGFP+ cells (16 ± 4% to 35 ± 3%), contrasting to a decrease in controls (22 ± 4% to 12 ± 4%), and the difference was significant for more than 3 months. A detailed study of lineage showed a preferential expansion of EGFP+ cells in granulocytes and monocytes following Tm administration. Conclusions Long-term repopulating cells were transduced with the SAG, and the transduced granulocyte/monocyte precursors were most likely to be expandable in vivo upon Tm stimulation. Copyright © 2002 John Wiley & Sons, Ltd. [source]

    Identification of the M-CSF Receptor in Endometriosis by Immunohistochemistry and RT-PCR

    AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 5 2004
    Liselotte Mettler
    Problem:, The aim of this paper is to provide further evidence that the dystopic proliferation of endometriotic epithelia is caused by the stimulation of peritoneal macrophages. It is essential to show that endometriotic epithelial cells express the macrophage colony-stimulating factor receptor (M-CSFR) which binds the M-CSF produced by the peritoneal macrophages. Method of study:, For the detection of M-CSFR, samples of ectopic endometrium (n = 79) and eutopic endometrium (n = 18) were compared. The specimens were gained at operative laparoscopy in the proliferative phase of the cycle. Cryostat sections were used for immunohistochemical detection. For in vitro reverse transcriptase polymerase chain reaction (RT-PCR) tests, the tissue was immediately shock frozen on paraffin sections. For the in situ RT-PCR technique the specimens were placed in a para-formaldehyde solution, embedded in paraffin and later processed. The Gene Amp 1000 in situ PCR system (Perkin Elmer) was used as the thermal cycler. Results:, M-CSF and the M-CSF receptor are present in eutopic and ectopic endometrium. Qualitatively, with both PCR techniques we found the M-CSF receptor to be present in all samples examined. Using the histochemical detection technique, the M-CSF receptor was found in nearly 70% of endometriosis patients compared with a statistically significant lower percentage in normal endometrium. Conclusions:, The in situ RT-PCR technique and immunohistochemistry elaborated the need to trace the cellular sources of the M-CSF receptor. The identification of the M-CSF receptor in endometriotic tissue and in endometrium is apt to open a new experimental field in endometriosis research. [source]

    Lack of detection of agonist activity by antibodies to platelet-derived growth factor receptor , in a subset of normal and systemic sclerosis patient sera

    ARTHRITIS & RHEUMATISM, Issue 4 2009
    Nick Loizos
    Objective To investigate whether agonist anti,platelet-derived growth factor receptor , (anti-PDGFR,) antibodies are present in the serum of patients with systemic sclerosis (SSc; scleroderma). Methods Sera were obtained from healthy subjects and scleroderma patients. An electrochemiluminescence binding assay was performed for detection of serum autoantibodies to PDGFR,, PDGFR,, epidermal growth factor receptor (EGFR), and colony-stimulating factor receptor 1 (CSFR1). Serum immunoglobulin was purified by protein A/G chromatography. To assess Ig agonist activity, PDGFR,-expressing cells were incubated with pure Ig and the level of receptor phosphorylation determined in an enzyme-linked immunoassay, as well as by Western blotting. Ig agonist activity was also assessed in a mitogenic assay and by MAP kinase activation in a PDGFR,-expressing cell line. Results Sera from 34.3% of the healthy subjects and 32.7% of the SSc patients contained detectable autoantibodies to PDGFR, and PDGFR,, but not EGFR or CSFR1. Purified Ig from these sera was shown to retain PDGFR binding activity and, at 200-1,000 ,g/ml, exhibited no agonist activity in a cell-based PDGFR, phosphorylation assay and did not stimulate a mitogenic response or MAP kinase activation in a PDGFR,-expressing cell line. Two purified Ig samples that were unable to bind PDGFR, did exhibit binding activity to a nonglycosylated form of PDGFR,. Conclusion Although approximately one-third of sera from scleroderma patients contained detectable autoantibodies to PDGFR, these antibodies were not specific to scleroderma, since they were also detected in a similar percentage of samples from normal subjects. PDGFR, agonist activity was not demonstrated when purified Ig from these sera was tested in cell-based assays. [source]

    Clonogenicity, gene expression and phenotype during neutrophil versus erythroid differentiation of cytokine-stimulated CD34+ human marrow cells in vitro

    BRITISH JOURNAL OF HAEMATOLOGY, Issue 4 2004
    Louise Edvardsson
    Summary With the objective to correlate clonogenicity, gene expression and phenotype during differentiation, human bone marrow CD34+ cells were cultured in vitro to stimulate erythroid or neutrophil development, and sorted into five subpopulations according to their surface expression of CD15/CD33 and blood group antigen A/CD117 respectively. Sorted cells were cultured in methylcellulose and analysed by real-time reverse transcription polymerase chain reaction for expression of neutrophil and erythroid marker genes. Surface expression of CD15 coincided with restriction to neutrophil/monocyte differentiation and A antigen with restriction to erythroid differentiation. GATA-2 mRNA was down-regulated during both neutrophil and erythroid maturation, whereas GATA-1, SCL, ABO, erythropoietin receptor, Kell, glycophorin A, , -globin and , -haemoglobin stabilizing protein were up-regulated during erythroid differentiation and silenced during neutrophil differentiation. CCAAT/enhancer-binding protein (C/EBP)- ,, PU.1, granulocyte colony-stimulating factor receptor, PR3, C/EBP- , and lactoferrin were sequentially expressed during neutrophil differentiation but rapidly down-regulated during the early erythroid stages. Nuclear factor erythroid-derived 2 (NF-E2) and glycophorin C were expressed both during neutrophil and erythroid differentiation. Our data support the notion of early expression of several lineage-associated genes prior to actual lineage commitment, defined by surface expression of CD15 and A antigen as markers for definitive neutrophil/monocyte and erythroid differentiation respectively. Previous findings, primarily from cell lines and mouse models, have been extended to adult human haematopoiesis. [source]