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  Indian J Med Microbiol
 

Figure 1: Granulocyte colony-stimulating factor stimulates hematopoietic stem cell mobilization by cleaving the retention axes, downregulating stromal-derived factor-1 expression, opening the endothelial boundaries, and counteracting the function of CXC chemokine receptor-4 through erythroblasts-derived fibroblast growth factor 23. In the steady state, hematopoietic stem cells are located and retained in bone marrow through several retention axes, such as SCF/c-kit, vascular cell adhesion molecule 1/VLA-4, and stromal-derived factor-1/CXC chemokine receptor-4 between hematopoietic stem cells and niche cells (a). Upon granulocyte colony-stimulating factor treatment, neutrophils secrete proteases, such as neutrophil elastase, cathepsin G, dipeptidyl peptidase I, and matrix metalloprotease 9, to cleave the retention axes (b). Granulocyte colony-stimulating factor induces sympathetic neurons to secrete noradrenaline and macrophages to secrete unknown factors to suppress stromal-derived factor-1 expression on the surface of niche cells (c). Granulocyte colony-stimulating factor increases CD26 on the surface of endothelial cells and then cleaves the N-terminal of NPY. Truncated NPY then binds the receptors on the surface of endothelial cells, downregulates VE-cadherin, and opens endothelial boundaries (d). Granulocyte colony-stimulating factor triggers erythroblasts to secrete fibroblast growth factor 23 and then counteract the function of CXC chemokine receptor-4 (e).

Figure 1: Granulocyte colony-stimulating factor stimulates hematopoietic stem cell mobilization by cleaving the retention axes, downregulating stromal-derived factor-1 expression, opening the endothelial boundaries, and counteracting the function of CXC chemokine receptor-4 through erythroblasts-derived fibroblast growth factor 23. In the steady state, hematopoietic stem cells are located and retained in bone marrow through several retention axes, such as SCF/c-kit, vascular cell adhesion molecule 1/VLA-4, and stromal-derived factor-1/CXC chemokine receptor-4 between hematopoietic stem cells and niche cells (a). Upon granulocyte colony-stimulating factor treatment, neutrophils secrete proteases, such as neutrophil elastase, cathepsin G, dipeptidyl peptidase I, and matrix metalloprotease 9, to cleave the retention axes (b). Granulocyte colony-stimulating factor induces sympathetic neurons to secrete noradrenaline and macrophages to secrete unknown factors to suppress stromal-derived factor-1 expression on the surface of niche cells (c). Granulocyte colony-stimulating factor increases CD26 on the surface of endothelial cells and then cleaves the N-terminal of NPY. Truncated NPY then binds the receptors on the surface of endothelial cells, downregulates VE-cadherin, and opens endothelial boundaries (d). Granulocyte colony-stimulating factor triggers erythroblasts to secrete fibroblast growth factor 23 and then counteract the function of CXC chemokine receptor-4 (e).