Change in the accessibility of an epitope of the human granulocyte-colony stimulating factor after binding to receptors

Marino, Julieta; Sterin-Prync, Aída; Roguin, Leonor P.

doi:10.1016/s1043-4666(03)00099-1

Cited by 6 publications

(8 citation statements)

References 30 publications

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“…5B). Effect of G-CSF on JEG-3 Cell Viability G-CSF induces a proliferative response in NFS-60 cells [Hara et al, 1988;Marino et al, 2003]. Under our experimental conditions, NFS-60 cell growth increased in a dose-dependent manner up to a concentration of 0.1 ng/ml of G-CSF (data not shown).…”

Section: G-csf Stimulates Map Kinase Phosphorylation In Jeg-3 Cellsmentioning

confidence: 47%

The granulocyte colony stimulating factor (G‐CSF) activates Jak/STAT and MAPK pathways in a trophoblastic cell line

Marino

Roguin

2007

J of Cellular Biochemistry

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Granulocyte colony-stimulating factor receptor (G-CSFR) has been found in placenta tissues, although its functional role has not yet been defined. In order to explore the molecular pathways induced by G-CSF in this tissue, we first reveal the presence of G-CSFR in the JEG-3 human trophoblastic cell line and then examined the phosphorylation of Janus tyrosine kinases (Jak), signal transducers and activators of transcription (STAT) proteins and mitogen-activated protein kinases (MAPK) after G-CSF binding to receptors. We showed that Jak1, Jak2, Tyk2, and STAT3 were phosphorylated after incubation with G-CSF. Phosphorylation of p38 and p44/42 MAPK was also activated by G-CSF, and specifically blocked in the presence of the corresponding inhibitors. Similar intracellular pathways were induced by G-CSF in a myeloid leukemia NFS-60 cell line that was studied in parallel. Conversely to cytokine action in myeloid cells, G-CSF did not induce a proliferative response in JEG-3 cells. When the effect of G-CSF on cellular viability was evaluated, cytokine-stimulated JEG-3 cells were protected from foetal serum starvation. In addition, when JEG-3 cells deprived of serum were incubated at different times in the presence of G-CSF, a progressive decrease in the percentage of hypodiploid cells was observed. In summary, we identified the molecular pathways activated after G-CSF binding to trophoblastic cell receptors and showed that G-CSF behaved as a protective cytokine, which supports JEG-3 cells survival.

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Section: G-csf Stimulates Map Kinase Phosphorylation In Jeg-3 Cellsmentioning

confidence: 47%

The granulocyte colony stimulating factor (G‐CSF) activates Jak/STAT and MAPK pathways in a trophoblastic cell line

Marino

Roguin

2007

J of Cellular Biochemistry

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“…However, recombinant G-CSF is cleared rapidly from the body and is administered to patients by daily subcutaneous injection. Therefore, the development of methods to prolong the circulating half-life and the potential therapeutic effectiveness of G-CSF is of interest to patients and healthcare providers [43]. The binding of G-CSF to heparin might result in several significant effects.…”

Section: Introductionmentioning

confidence: 99%

Separation, identification, and interaction of heparin oligosaccharides with granulocyte-colony stimulating factor using capillary electrophoresis and mass spectrometry

et al. 2005

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A capillary electrophoresis (CE) method was developed for the separation of heparin oligosaccharides compatible to study the interactions between the oligosaccharides and granulocyte-colony stimulating factor (G-CSF). Unfractionated heparin was eliminitively degraded to heparin oligosaccharides by an endolytic heparinase. The degraded smaller oligosaccharides (M(r) < 1000) were baseline-separated by CE under a 50 mM phosphate buffer (pH 9.0) in 10 min. Standard heparin disaccharides and larger oligosaccharides (1000 < M(r) < 8000) were all separated under optimized separation conditions. Compared with standard heparin disaccharides, smaller oligosaccharides contained one nonsulfated, two monosulfated, and two disulfated disaccharides, but trisulfated disaccharides were not found. The smaller oligosaccharides were also identified and molecular mass was deduced by electrospray ionization-mass spectrometry (ESI-MS). Furthermore, interactions between G-CSF and the oligosaccharides were studied by using capillary zone electrophoresis (CZE) under the above separation conditions. It was found that larger oligosaccharides could interact with G-CSF while smaller oligosaccharides were not observed to bind to G-CSF under the experimental conditions. In conclusion, the purified heparinase could selectively degrade heparin into oligosaccharides and the interaction between G-CSF and heparin was correlated with the chain length of heparin.

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“…G-CSF is currently used clinically to reduce the risk of life-threatening infection in patients with neutropenia, particularly after intense cytotoxic chemotherapy, radiotherapy, and bone marrow transplantation [25,26]. Previously, using CZE and single molecules detection methods, it was found that G-CSF could interact with heparin [29,30] and the interaction was dependent on heparin chain length [31].…”

Section: Introductionmentioning

confidence: 99%

Further characterization of the binding of heparin to granulocyte colony‐stimulating factor: Importance of sulfate groups

Liang

Liu

et al. 2008

Electrophoresis

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Heparin mediates fundamental biological mechanisms through interaction with proteins. Previously, we have shown that standard heparin binds to granulocyte colony-stimulating factor (G-CSF) with an affinity of 4.8 x 10(5) M(-1). To further study the structural features in heparin that are responsible for this interaction, we studied the bindings of G-CSF and N-desulfated and 2,3-O-desulfated heparin by CZE. Results showed that the N-desulfated heparin had a similar affinity for G-CSF ((5.4 +/- 0.9) x 10(5) M(-1)), but the 2,3-O-desulfated heparin had a 1000-fold lower affinity ((3.4 +/- 1.2) x 10(2) M(-1)) in comparison to standard heparin. The results showed that 2,3-O-sulfate groups are more important than N-sulfate groups in heparin-G-CSF interaction.

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Change in the accessibility of an epitope of the human granulocyte-colony stimulating factor after binding to receptors

Cited by 6 publications

References 30 publications

The granulocyte colony stimulating factor (G‐CSF) activates Jak/STAT and MAPK pathways in a trophoblastic cell line

The granulocyte colony stimulating factor (G‐CSF) activates Jak/STAT and MAPK pathways in a trophoblastic cell line

Separation, identification, and interaction of heparin oligosaccharides with granulocyte-colony stimulating factor using capillary electrophoresis and mass spectrometry

Further characterization of the binding of heparin to granulocyte colony‐stimulating factor: Importance of sulfate groups

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