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COLONY STIMULATING FACTOR 2
LATEST LITERATURE
1: Oral diseases, 2010 Mar 9,
In vivo expression of Toll-like receptor 2, Toll-like receptor 4, CSF2 and LY64 in Chinese chronic periodontitis patients.
[Abstract]Oral Diseases (2010) doi: 10.1111/j.1601-0825.2009.01630.x Objective: Toll-like receptors (TLRs) are the essential components in the innate and adaptive immune systems. Colony stimulating factor 2 (CSF2) is a cytokine that may prevent endotoxin tolerance, and LY64 has the ability to interfere with the recognition of bacteria via TLR4. The aim of this study was to explore the in vivo expressions of TLR2, TLR4, CSF2 and LY64 in Chinese chronic periodontitis patients. Methods: Gingival biopsies were collected from 24 chronic periodontitis patients and 19 healthy controls. The gene expression profiles of TLR2, TLR4, CSF2 and LY64 were investigated by real-time polymerase chain reaction, and the protein expressions of TLR2 and TLR4 were detected by immunohistochemistry. In addition, the levels of CSF2 in gingival crevicular fluid (GCF) were determined by ELISA. Results: The higher mRNA expressions of TLR2, TLR4 and CSF2, and the lower mRNA expression of LY64 were detected in chronic periodontitis patients. And the increased protein expressions of TLR2 and TLR4 were confirmed by immunohistochemistry. In addition, the increase of total amount of CSF2 in GCF was observed in chronic periodontitis patients. Conclusions: Our results suggest that TLR2 and TLR4 may play a role in periodontal pathogenesis. In addition, CSF2 and LY64 may contribute to the regulation of inflammatory response and maintaining periodontal homeostasis.
2: Endocrinology, 2009 Nov, 150(11)
Colony-Stimulating Factor 2 (CSF-2) Improves Development and Posttransfer Survival of Bovine Embryos Produced in Vitro.
[Abstract]In this study, we tested the role of colony-stimulating factor 2 (CSF2) as one of the regulatory molecules that mediate maternal effects on embryonic development during the preimplantation period. Our objective was to verify effects of CSF2 on blastocyst yield, determine posttransfer survival, and evaluate properties of the blastocyst formed after CSF2 treatment. In vitro, CSF2 increased the percentage of oocytes that became morulae and blastocysts. Blastocysts that were treated with CSF2 tended to have a greater number of inner cell mass cells and had a higher ratio of inner cell mass to trophectoderm cells. There was no effect of CSF2 on the incidence of apoptosis. Treatment with CSF2 from d 5 to 7 after insemination increased embryonic survival as indicated by improved pregnancy rate at d 30-35 of gestation. Moreover, treatment with CSF2 from either d 1-7 or 5-7 after insemination reduced pregnancy loss after d 30-35. Results indicate that treatment with CSF2 can affect embryonic development and enhance embryo competence for posttransfer survival. The fact that treatment with CSF2 during such a narrow window of development altered embryonic function much later in pregnancy suggests that CSF2 may exert epigenetic effects on the developing embryo that result in persistent changes in function during the embryonic and fetal periods of development.
3: Biology of reproduction, 2009 Feb 18,
Csf2 Null Mutation Alters Placental Gene Expression and Trophoblast Glycogen Cell and Giant Cell Abundance in Mice.
[Abstract]Genetic deficiency in granulocyte-macrophage colony-stimulating factor (CSF2, GM-CSF) results in altered placental structure in mice. To investigate the mechanism of action of CSF2 in placental morphogenesis, placental gene expression and cell composition were examined in Csf2 null mutant and wild-type mice. Microarray and qRT-PCR analyses on E13 placentae revealed that Csf2 null mutation caused altered expression of seventeen genes not previously associated with placental development including Mid1, Cd24a, Tnfrsf11b, and Wdfy1. Genes controlling trophoblast differentiation Ascl2, Tcfeb, Itgav, and Socs3 were also differentially expressed. CSF2 ligand and the CSF2 receptor alpha-subunit (CSF2RA) were predominantly synthesized in the placental junctional zone. Altered placental structure in Csf2 null mice at E15 was characterized by an expanded junctional zone and increased Cx31(+) glycogen cells and CDKN1C(+) (P57(Kip2+)) giant cells, accompanied by elevated junctional zone transcription of genes controlling spongiotrophoblast and giant cell differentiation and secretory function, Ascl2, Hand1, Prl3d1 and Prl2c2. Granzyme genes implicated in tissue remodeling and potentially in trophoblast invasion, Gzmc, Gzme and Gzmf, were downregulated in junctional zone of Csf2 null mutant placentae. These data demonstrate aberrant placental gene expression in Csf2 null mutant mice associated with altered differentiation and/or functional maturation of the junctional zone trophoblast lineages, glycogen cells and giant cells. We conclude that CSF2 is a regulator of trophoblast differentiation and placental development which potentially influences the functional capacity of the placenta to support optimal fetal growth in pregnancy.
4: Reproductive sciences (Thousand Oaks, Calif.), 2009 Jan 30,
Mechanisms of Leukocyte Accumulation and Activation in Chorioamnionitis: Interleukin 1B and Tumor Necrosis Factor Enhance Colony Stimulating Factor 2 Expression in Term Decidua.
[Abstract]Chorioamnionitis is a major cause of prematurity as well as perinatal morbidity and mortality. The present study observed a marked increase in immunohistochemical staining for Colony Stimulating Factor 2 (CSF2; also known as granulocyte macrophage-colony stimulating factor), a potent neutrophil and macrophage chemoattractant and activator, in the decidua of patients with CAM compared with controls (n = 8; P = .001). To examine the regulation of this CSF2, cultured decidual cells primed with estradiol (E2) or E2 plus medroxyprogesterone acetate, were exposed to tumor necrosis factor-alpha or interleukin-1beta and secreted CSF2 measured by ELISA. Levels of CSF2 in E2 plus MPA-treated cultures increased 18- and 245-fold following treatment with TNF or IL1B (n = 7, P < .05). Quantitative RT-PCR demonstrated parallel changes in mRNA levels. This study reveals that CSF2 is strongly expressed in decidua from patients with CAM and indicates TNF or IL1B as important regulators of CAM-related decidual leukocyte infiltration and activation.
5: Journal of autoimmunity, 2008 Dec, 31(4)
GM-CSF induces STAT5 binding at epigenetic regulatory sites within the Csf2 promoter of non-obese diabetic (NOD) mouse myeloid cells.
[Abstract]Myeloid cells from non-obese diabetic (NOD) mouse and human type 1 diabetic (T1D) patients overexpress granulocyte-macrophage colony stimulation factor (GM-CSF). This overproduction prolongs the activation of signal transduction and activator of transcription 5 (STAT5) proteins, involved in GM-CSF-induced control of myeloid cell gene expression. We found that GM-CSF can regulate the binding of STAT5 on the promoter of its own gene, Csf2, within regions previously identified as sites of chromatin epigenetic modification important to the regulation of GM-CSF during myeloid differentiation and inflammation. We found multiple sequence polymorphisms within NOD mouse chromosome 11 Idd4.3 diabetes susceptibility region that alter STAT5 GAS binding sequences within the Csf2 promoter. STAT5 binding at these sites in vivo is increased significantly in GM-CSF-stimulated-bone marrow cells and in unactivated, high GM-CSF-producing macrophages from NOD mice as compared to non-autoimmune C57BL/6 mouse myeloid cells. Thus, GM-CSF overproduction by NOD myeloid cells may be perpetuating a positive epigenetic regulatory feedback on its own gene expression through its induction of STAT5 binding to its promoter. These findings suggest that aberrant STAT5 binding at epigenetic regulatory sites may contribute directly to immunopathology through cytokine-induced gene expression dysregulation that can derail myeloid differentiation and increase inflammatory responsiveness.
6: The European respiratory journal : official journal of the European Society for Clinical Respiratory Physiology, 2008 Jul, 32(1)
Association of genetic variations in the CSF2 and CSF3 genes with lung function in smoking-induced COPD.
[Abstract]Granulocyte-macrophage colony-stimulating factor (CSF), also known as CSF2, and granulocyte CSF, also known as CSF3, are important survival and proliferation factors for neutrophils and macrophages. The objective of the present study was to determine whether single nucleotide polymorphisms (SNPs) of CSF2 and CSF3 are associated with lung function in smoking-induced chronic obstructive pulmonary disease. In total, five SNPs of CSF2 and CSF3 were studied in 587 non-Hispanic white subjects with the fastest (n = 281) or the slowest (n = 306) decline of lung function selected from among continuous smokers in the National Heart, Lung, and Blood Institute Lung Health Study (LHS). These SNPs were also studied in 1,074 non-Hispanic white subjects with the lowest (n = 536) or the highest (n = 538) baseline lung function at the beginning of the LHS. An increase in the number of CSF3 -1719T alleles was significantly associated with protection against low lung function (odds ratio 0.73, 95% confidence interval 0.56-0.95), and was still significant after adjustment for multiple comparisons. There was also a significant association of a CSF3 haplotype with baseline levels of forced expiratory volume in one second. No association was found for CSF2 SNPs and lung function, nor was there evidence of epistasis. In conclusion, genetic variation in colony-stimulating factor 3 is associated with cross-sectionally measured lung function in smokers.
7: Journal of human genetics, 2001, 46(1)
Novel single nucleotide polymorphisms of the human colony-stimulating factor 2 (CSF2) gene identified by sequencing the entire gene.
[Abstract]We describe three single nucleotide polymorphisms (SNPs) of the human colony-stimulating factor 2 (CSF2) gene and their allelic frequencies, as determined by direct sequencing of 48 alleles of the entire CSF2 gene. Three polymorphisms were identified, at nucleotide positions 1816 (T/C), 2284 (C/T), and 3079 (G/A). These polymorphisms will be useful in genetic studies not only of hematologic disorders but also of disorders of bone metabolism.
8: Mammalian genome : official journal of the International Mammalian Genome Society, 1996 Nov, 7(11)
Mapping the ovine genes encoding IL3, IL4, IL5, and CSF2 to sheep chromosome 5q13-q15 by FISH.
[Abstract]We describe three single nucleotide polymorphisms (SNPs) of the human colony-stimulating factor 2 (CSF2) gene and their allelic frequencies, as determined by direct sequencing of 48 alleles of the entire CSF2 gene. Three polymorphisms were identified, at nucleotide positions 1816 (T/C), 2284 (C/T), and 3079 (G/A). These polymorphisms will be useful in genetic studies not only of hematologic disorders but also of disorders of bone metabolism.
9: Journal of immunology (Baltimore, Md. : 1950), 1985 Jul, 135(1)
Generation of anti-peptide monoclonal antibodies which recognize mature CSF-2 alpha (IL 3) protein.
[Abstract]The colony-stimulating factor CSF-2 alpha (IL 3) has been purified to homogeneity, the protein sequenced, and the gene encoding this lymphokine cloned. Knowledge of the protein sequence permitted the synthesis of peptides corresponding to the amino terminus of the molecule. These peptides, after conjugation to palmitic acid, were used to immunize mice. Spleen cells from mice immunized with one of these peptides (CSF-2 alpha 1-14) were fused with the myeloma cell line NS-1. The fusion resulted in the isolation of two hybridoma cell lines, designated 6A5 and 4D4, that secreted antibodies that were specific for the immunizing peptide. The antibodies did not react with a closely related peptide CSF-2 alpha 7-16. The antibodies were capable, however, of recognized CSF-2 alpha protein as judged by the ability of the antibodies to remove CSF-2 alpha activity from culture medium of PHA-stimulated LBRM-33-5A4 cells, to immunoprecipitate radiolabeled CSF-2 alpha protein, and to detect CSF-2 alpha protein bound to nitrocellulose membranes.
10: The Journal of biological chemistry, 1986 Jan 5, 261(1)
Characterization of the cell surface receptor for a multi-lineage colony-stimulating factor (CSF-2 alpha).
[Abstract]125I-Labeled colony-stimulating factor (CSF) 2 alpha (interleukin 3, multi-CSF, and mast cell growth factor) was used to characterize receptors specific for this lymphokine on the cell surface of the factor-dependent cell line FDC-P2. CSF-2 alpha binding to these cells was specific and saturable. Among a panel of lymphokines and growth factors, only unlabeled CSF-2 alpha was able to compete for the binding of 125I-labeled CSF-2 alpha to cells. Equilibrium binding studies revealed that CSF-2 alpha bound to 434 +/- 281 receptors/cell with a Ka of 8.7 +/- 3.9 X 10(9) M-1. Affinity cross-linking experiments with the homobifunctional cross-linking reagents disuccinimidyl suberate, disuccinimidyl tartrate, and dithiobis(succinimidyl propionate) produced a radiolabeled band of Mr = 97,000 on intact cells and in purified cell membranes, while an additional band of Mr = 138,000 was produced upon cross-linking to intact cells only. The relationship between these two bands is discussed. The results indicate that the receptor for CSF-2 alpha on FDC-P2 cells consists at a minimum of a subunit of Mr = 72,500.
11: The New England journal of medicine, 1992 Jul 9, 327(2)
Granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor (2).
[Abstract]We describe three single nucleotide polymorphisms (SNPs) of the human colony-stimulating factor 2 (CSF2) gene and their allelic frequencies, as determined by direct sequencing of 48 alleles of the entire CSF2 gene. Three polymorphisms were identified, at nucleotide positions 1816 (T/C), 2284 (C/T), and 3079 (G/A). These polymorphisms will be useful in genetic studies not only of hematologic disorders but also of disorders of bone metabolism.