scholarly journals Colony-Stimulating Factor-1-Responsive Macrophage Precursors Reside in the Amphibian (Xenopus laevis) Bone Marrow rather than the Hematopoietic Subcapsular Liver

2013 ◽  
Vol 5 (6) ◽  
pp. 531-542 ◽  
Author(s):  
Leon Grayfer ◽  
Jacques Robert
Keyword(s):  
Bone Marrow ◽  
Xenopus Laevis ◽  
Colony Stimulating Factor ◽  
Stimulating Factor ◽  
Macrophage Precursors

scholarly journals Investigating the Possibility of Intervertebral Disc Regeneration Induced by Granulocyte Colony Stimulating Factor-Stimulated Stem Cells in Rats

2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Wen-Ching Tzaan ◽  
Hsien-Chih Chen
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Intervertebral Disc ◽  
Bone Marrow Stem Cells ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Hematopoietic Stem ◽  
Disc Regeneration ◽  
Intervertebral Disc Regeneration ◽  
Stimulating Factor

Intervertebral disc (IVD) degeneration is a multifactorial process that is influenced by contributions from genetic predisposition, the aging phenomenon, lifestyle conditions, biomechanical loading and activities, and other health factors (such as diabetes). Attempts to decelerate disc degeneration using various techniques have been reported. However, to date, there has been no proven technique effective for broad clinical application. Granulocyte colony-stimulating factor (GCSF) is a growth factor cytokine that has been shown to enhance the availability of circulating hematopoietic stem cells to the brain and heart as well as their capacity for mobilization of mesenchymal bone marrow stem cells. GCSF also exerts significant increases in circulating neutrophils as well as potent anti-inflammatory effects. In our study, we hypothesize that GCSF can induce bone marrow stem cells differentiation and mobilization to regenerate the degenerated IVD. We found that GCSF had no contribution in disc regeneration or maintenance; however, there were cell proliferation within end plates. The effects of GCSF treatment on end plates might deserve further investigation.

scholarly journals Congenital neutropenia: neutrophil proliferation with abnormal maturation

Blood ◽  
1975 ◽  
Vol 46 (5) ◽  
pp. 723-734 ◽  
Author(s):  
RT Parmley ◽  
M Ogawa ◽  
CP Jr Darby ◽  
SS Spicer
Keyword(s):  
Bone Marrow ◽  
Acid Phosphatase ◽  
Colony Stimulating Factor ◽  
Peripheral Blood Leukocytes ◽  
Congenital Neutropenia ◽  
Blood Leukocytes ◽  
Specific Granules ◽  
Primary Granules ◽  
Stimulating Factor ◽  
Myelin Figures

Abstract A child with congenital neutropenia was studied using bone marrow culture and ultrastructural and cytochemical techniques. The patient's marrow cells formed a large number of granulocytic colonies of normal size in culture, and her peripheral blood leukocytes produced adequate colony-stimulating factor. No serum inhibitors were identified. The patient's promyelocytes from direct marrow and culture appeared normal in ultrastructure, and primary granules, contained peroxidase and acid phosphatase activity. Myelocytes and rare segmented neutrophils from direct marrow specimens demonstrated atypical notched nuclei, myelin figures in Golgi lamellae and primary (azurophilic) granules, and no identifiable secondary (specific) granules. These data indicate an intrinsic neutrophil defect which allows normal proliferation of precursor cells, but results in abnormal granulogenesis and apparent inability to form secondary granules.

scholarly journals CXCR4 is a key regulator of neutrophil release from the bone marrow under basal and stress granulopoiesis conditions

Blood ◽  
2009 ◽  
Vol 113 (19) ◽  
pp. 4711-4719 ◽  
Author(s):  
Kyle J. Eash ◽  
Jacquelyn M. Means ◽  
Douglas W. White ◽  
Daniel C. Link
Keyword(s):  
Bone Marrow ◽  
Listeria Monocytogenes ◽  
Host Tissue ◽  
Microbial Pathogens ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Cxcr4 Signaling ◽  
Listeria Monocytogenes Infection ◽  
A Cell ◽  
Stimulating Factor

Abstract The number of neutrophils in the blood is tightly regulated to ensure adequate protection against microbial pathogens while minimizing damage to host tissue. Neutrophil homeostasis in the blood is achieved through a balance of neutrophil production, release from the bone marrow, and clearance from the circulation. Accumulating evidence suggests that signaling by CXCL12, through its major receptor CXCR4, plays a key role in maintaining neutrophil homeostasis. Herein, we generated mice with a myeloid lineage–restricted deletion of CXCR4 to define the mechanisms by which CXCR4 signals regulate this process. We show that CXCR4 negatively regulates neutrophil release from the bone marrow in a cell-autonomous fashion. However, CXCR4 is dispensable for neutrophil clearance from the circulation. Neutrophil mobilization responses to granulocyte colony-stimulating factor (G-CSF), CXCL2, or Listeria monocytogenes infection are absent or impaired, suggesting that disruption of CXCR4 signaling may be a common step mediating neutrophil release. Collectively, these data suggest that CXCR4 signaling maintains neutrophil homeostasis in the blood under both basal and stress granulopoiesis conditions primarily by regulating neutrophil release from the bone marrow.

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