scholarly journals Permissive role of thrombopoietin and granulocyte colony-stimulating factor receptors in hematopoietic cell fate decisions in vivo

1999 ◽  
Vol 96 (2) ◽  
pp. 698-702 ◽  
Author(s):  
R. Stoffel ◽  
S. Ziegler ◽  
N. Ghilardi ◽  
B. Ledermann ◽  
F. J. de Sauvage ◽  
...  
Keyword(s):  
Cell Fate ◽  
Hematopoietic Cell ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Cell Fate Decisions ◽  
Stimulating Factor ◽  
Permissive Role

scholarly journals Interleukin-6 and the Granulocyte Colony-Stimulating Factor Receptor Are Major Independent Regulators of Granulopoiesis In Vivo But Are Not Required for Lineage Commitment or Terminal Differentiation

Blood ◽  
1997 ◽  
Vol 90 (7) ◽  
pp. 2583-2590 ◽  
Author(s):  
Fulu Liu ◽  
Jennifer Poursine-Laurent ◽  
Huai Yang Wu ◽  
Daniel C. Link
Keyword(s):  
Interleukin 6 ◽  
Terminal Differentiation ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Normal Numbers ◽  
Stimulating Factor ◽  
Deficient Mice ◽  
Additional Loss

Multiple hematopoietic cytokines can stimulate granulopoiesis; however, their relative importance in vivo and mechanisms of action remain unclear. We recently reported that granulocyte colony-stimulating factor receptor (G-CSFR)-deficient mice have a severe quantitative defect in granulopoiesis despite which phenotypically normal neutrophils were still detected. These results confirmed a role for the G-CSFR as a major regulator of granulopoiesis in vivo, but also indicated that G-CSFR independent mechanisms of granulopoiesis must exist. To explore the role of interleukin-6 (IL-6) in granulopoiesis, we generated IL-6 × G-CSFR doubly deficient mice. The additional loss of IL-6 significantly worsened the neutropenia present in young adult G-CSFR–deficient mice; moreover, exogenous IL-6 stimulated granulopoiesis in vivo in the absence of G-CSFR signals. Near normal numbers of myeloid progenitors were detected in the bone marrow of IL-6 × G-CSFR–deficient mice and their ability to terminally differentiate into mature neutrophils was observed. These results indicate that IL-6 is an independent regulator of granulopoiesis in vivo and show that neither G-CSFR or IL-6 signals are required for the commitment of multipotential progenitors to the myeloid lineage or for their terminal differentiation.

scholarly journals Interleukin-6 and the Granulocyte Colony-Stimulating Factor Receptor Are Major Independent Regulators of Granulopoiesis In Vivo But Are Not Required for Lineage Commitment or Terminal Differentiation

Blood ◽  
1997 ◽  
Vol 90 (7) ◽  
pp. 2583-2590 ◽  
Author(s):  
Fulu Liu ◽  
Jennifer Poursine-Laurent ◽  
Huai Yang Wu ◽  
Daniel C. Link
Keyword(s):  
Interleukin 6 ◽  
Terminal Differentiation ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Normal Numbers ◽  
Stimulating Factor ◽  
Deficient Mice ◽  
Additional Loss

Abstract Multiple hematopoietic cytokines can stimulate granulopoiesis; however, their relative importance in vivo and mechanisms of action remain unclear. We recently reported that granulocyte colony-stimulating factor receptor (G-CSFR)-deficient mice have a severe quantitative defect in granulopoiesis despite which phenotypically normal neutrophils were still detected. These results confirmed a role for the G-CSFR as a major regulator of granulopoiesis in vivo, but also indicated that G-CSFR independent mechanisms of granulopoiesis must exist. To explore the role of interleukin-6 (IL-6) in granulopoiesis, we generated IL-6 × G-CSFR doubly deficient mice. The additional loss of IL-6 significantly worsened the neutropenia present in young adult G-CSFR–deficient mice; moreover, exogenous IL-6 stimulated granulopoiesis in vivo in the absence of G-CSFR signals. Near normal numbers of myeloid progenitors were detected in the bone marrow of IL-6 × G-CSFR–deficient mice and their ability to terminally differentiate into mature neutrophils was observed. These results indicate that IL-6 is an independent regulator of granulopoiesis in vivo and show that neither G-CSFR or IL-6 signals are required for the commitment of multipotential progenitors to the myeloid lineage or for their terminal differentiation.

P–391 Role of subcutaneous granulocyte colony-stimulating factor infusion in thin endometrium

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
K Banerjee ◽  
B Singla
Keyword(s):  
Pregnancy Rate ◽  
Clinical Pregnancy ◽  
P Value ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Thin Endometrium ◽  
Group 2 ◽  
Stimulating Factor ◽  
Group 1

Abstract Study question To assess the role of subcutaneous granulocyte colony-stimulating factor (G-CSF) in thin endometrium cases. Summary answer G CSF has beneficial role to improve the endometrium thickness in thin endometrium. What is known already Endometrium is very important for embryo implantation and the endometrial thickness is the marker of receptivity of the endometrium. Study design, size, duration Study design - Retrospective analysis Size - 88 infertile females with thin endometrium (< 7 mm) in the age group of 23 to 40 years Duration - one year. Participants/materials, setting, methods In the group 1 of 44 females, subcutaneous infusion of G CSF (300 mcg/ml) was added along with other supplements and if lining was not more than 7 mm in 72 hours, then second infusion was given. In the group 2 of 44 females, only estradiol valerate and sildenafil were given.The efficacy of G CSF was evaluated by assessing the endometrium thickness before embryo transfer, pregnancy rates and clinical pregnancy rates. Main results and the role of chance There was no difference between the two groups regarding demographic variables, egg reserve, sperm parameters, number of embryos transferred and embryo quality. . The pregnancy rate was 60% (24 out of 40 cases) in the group 1 that was significantly higher than in-group 2 that was 31% (9 out of 29 cases) with p value < 0.0001. The clinical pregnancy rate was also significantly higher in-group 1 (55%) as compared to group 2 (24%) with p value < 0.0001. Limitations, reasons for caution Further larger cohort studies are required to explore the subcutaneous role of G CSF in thin endometrium. Wider implications of the findings: Granulocyte colony-stimulating factor has beneficial role to improve the endometrium thickness in thin endometrium. In most of previous studies, the intrauterine infusion of G CSF was given to improve the uterine lining. This is one of the few studies done that showed subcutaneous role of G CSF in thin endometrium. Trial registration number Not applicable

scholarly journals A comparison of hematopoiesis in normal and splenectomized mice treated with granulocyte colony-stimulating factor

Blood ◽  
1990 ◽  
Vol 75 (3) ◽  
pp. 563-569 ◽  
Author(s):  
G Molineux ◽  
Z Pojda ◽  
TM Dexter
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Extramedullary Hematopoiesis ◽  
High Dose ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Response Data ◽  
Hematopoietic Precursor ◽  
Stimulating Factor

Abstract Recombinant human granulocyte colony-stimulating factor (rhG-CSF) induces leukocytosis in vivo in both intact and splenectomized mice. Full dose response data showed a plateau in this effect at doses over 500 micrograms rhG-CSF/kg body weight/d in intact mice. The effect is magnified in splenectomized mice, where leukocyte numbers reach 100 x 10(6) mL after 4 days' treatment at 250 micrograms/kg/d. Further hematopoietic precursor populations are also affected in both marrow and the spleen; in general, marrow parameters were depressed, while splenic populations were enlarged. In splenectomized mice, both blood- borne stem cells were enhanced, and foci of extramedullary hematopoiesis were enlarged in addition to the effects seen in intact mice. In the marrow of splenectomized and intact mice treated with a high dose of G-CSF, erythroid suppression in the marrow was confirmed with radioactive iron. Our studies confirm and extend previous work on the mode of action of G-CSF, and indicate that side effects of high dose G-CSF therapy might include erythroid suppression in the bone marrow.

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