Amyloid-β peptides induce cell proliferation and macrophage colony-stimulating factor expression via the PI3-kinase/Akt pathway in cultured Ra2 microglial cells

FEBS Letters ◽  
2005 ◽  
Vol 579 (9) ◽  
pp. 1995-2000 ◽  
Author(s):  
Sachiko Ito ◽  
Makoto Sawada ◽  
Masataka Haneda ◽  
Satoshi Fujii ◽  
Kentaro Oh-hashi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Amyloid Β ◽  
Pi3 Kinase ◽  
Akt Pathway ◽  
Colony Stimulating Factor ◽  
Factor Expression ◽  
Macrophage Colony Stimulating Factor ◽  
Induce Cell Proliferation ◽  
Macrophage Colony ◽  
Stimulating Factor

The granulocyte macrophage colony stimulating factor (GM-CSF) regulates amyloid β (Aβ) production

Cytokine ◽  
2008 ◽  
Vol 42 (3) ◽  
pp. 336-344 ◽  
Author(s):  
Claude-Henry Volmar ◽  
Ghania Ait-Ghezala ◽  
Jeremy Frieling ◽  
Daniel Paris ◽  
Michael J. Mullan
Keyword(s):  
Amyloid Β ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Aβ Production ◽  
Stimulating Factor

scholarly journals Recombinant human interleukin-3 and recombinant human granulocyte- macrophage colony-stimulating factor administered in vivo after high- dose cyclophosphamide cancer chemotherapy: effect on hematopoiesis and microenvironment in human bone marrow

Blood ◽  
1992 ◽  
Vol 79 (10) ◽  
pp. 2610-2619 ◽  
Author(s):  
A Orazi ◽  
G Cattoretti ◽  
R Schiro ◽  
S Siena ◽  
M Bregni ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Proliferation ◽  
Endothelial Cell Proliferation ◽  
Control Group ◽  
High Dose ◽  
Colony Stimulating Factor ◽  
Interleukin 3 ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

The effects on bone marrow (BM) cell proliferation and differentiation of recombinant human interleukin-3 (rhIL-3) and recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) administered after high-dose (7 g/m2/d) cyclophosphamide (HD-CTX) chemotherapy were studied in nine patients with malignancies without BM involvement and in three control patients. rhIL-3 at a dose of 1 to 5 micrograms/kg/day was administered for 14 to 18 days by continuous intravenous (i.v.) infusion and rhGM-CSF was administered at a dose of 5.5 micrograms/kg/day for 14 days. Changes induced by cytokine treatment were assessed by morphoimmunohistochemical analysis of BM biopsies. Comparison was made in the cytokine-treated groups and with control patients who received HD-CTX alone. BM cellularity and the myeloid/erythroid (ME) ratio were lower in rhIL-3-treated than in rhGM- CSF-treated patients, but in both groups it was significantly higher than in the controls. The proportion of BM cells stained by PC10, a monoclonal antibody (MoAb) recognizing a proliferation-associated nuclear protein (PCNA), increased from 6.78% to 21.18% (P less than .02) after rhIL-3, and from 5% to 35.33% (P less than .001) after rhGM- CSF; no increase was observed in the control group. The frequency of CD34+ BM cells was unchanged after rhIL-3 (P = NS) and decreased after rhGM-CSF (P less than .001). In both groups, most of the PC10+ cells were represented by promyelocytes and myelocytes with no increase in blast cell numbers. rhIL-3-treated BM showed an increased number of megakaryocytes and increased proliferative activity of erythroid cells as compared with rhGM-CSF cases. BM stroma changes observed in both treated groups included endothelial cell proliferation, increased BM macrophage concentration, and increase in BM fibroblasts as detected with an anti-nerve growth factor receptor antibody. In most rhIL-3- treated cases, BM fibrosis developed after treatment. The same effect was not observed in rhGM-CSF patients.

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