scholarly journals Platelet-derived growth factor BB mediates the glioma-induced migration of bone marrow-derived mesenchymal stem cells by promoting the expression of vascular cell adhesion molecule-1 through the PI3K, P38 MAPK and NF-κB pathways

2013 ◽  
Vol 30 (6) ◽  
pp. 2755-2764 ◽  
Author(s):  
YI HU ◽  
PENG CHENG ◽  
JIANG-CHUN MA ◽  
YI-XUE XUE ◽  
YUN-HUI LIU
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Cell Adhesion ◽  
Growth Factor ◽  
Cell Adhesion Molecule ◽  
Platelet Derived Growth Factor ◽  
Vascular Cell Adhesion ◽  
Vascular Cell ◽  
Cell Adhesion Molecule 1

Vascular cell adhesion molecule-1 (CD106) is cleaved by neutrophil proteases in the bone marrow following hematopoietic progenitor cell mobilization by granulocyte colony-stimulating factor

Blood ◽  
2001 ◽  
Vol 98 (5) ◽  
pp. 1289-1297 ◽  
Author(s):  
Jean-Pierre Lévesque ◽  
Yasushi Takamatsu ◽  
Susan K. Nilsson ◽  
David N. Haylock ◽  
Paul J. Simmons
Keyword(s):  
Bone Marrow ◽  
Cell Adhesion ◽  
Cell Adhesion Molecule ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Vascular Cell Adhesion ◽  
Hematopoietic Progenitor ◽  
Vascular Cell ◽  
Cell Adhesion Molecule 1 ◽  
Stimulating Factor

Mobilized progenitor cells currently represent the most commonly used source of hematopoietic progenitor cells (HPCs) to effect hematopoietic reconstitution following myeloablative chemotherapies. Despite their widespread use, the molecular mechanisms responsible for the enforced egress of HPCs from the bone marrow (BM) into the circulation in response to mobilizing agents such as cytokines remain to be determined. Results of this study indicate that expression of vascular cell adhesion molecule-1 (VCAM-1) is strongly reduced in vivo in the BM during HPC mobilization by granulocyte colony-stimulating factor (G-CSF) and stem cell factor. Two serine proteases, namely, neutrophil elastase and cathepsin G, were identified, which cleave VCAM-1 and are released by neutrophils accumulating in the BM during the course of immobilization induced by G-CSF. The proposal is made that an essential step contributing to the mobilization of HPCs is the proteolytic cleavage of VCAM-1 expressed by BM stromal cells, an event triggered by the degranulation of neutrophils accumulating in the BM in response to the administration of G-CSF.

scholarly journals Vascular cell adhesion molecule-1 expressed by bone marrow stromal cells mediates the binding of hematopoietic progenitor cells

Blood ◽  
1992 ◽  
Vol 80 (2) ◽  
pp. 388-395 ◽  
Author(s):  
PJ Simmons ◽  
B Masinovsky ◽  
BM Longenecker ◽  
R Berenson ◽  
B Torok-Storb ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Stromal Cells ◽  
Cell Adhesion Molecule ◽  
Marrow Stromal Cells ◽  
Vascular Cell Adhesion ◽  
Vascular Cell ◽  
Cd34 Cells ◽  
Cell Adhesion Molecule 1

Human bone marrow-derived CD34+ cells were analyzed for the expression of the beta 1-family of integrin adhesion molecules. Integrin alpha 4 beta 1 was consistently expressed by greater than 90% of CD34+ cells, including essentially all assayable granulocyte-macrophage colony- forming cells (CFU-GM) and erythroid bursts (BFU-E) as shown by fluorescence-activated cell sorting studies. Adhesion of highly enriched CD34+ cells to cultured allogeneic marrow stromal cells was largely inhibited both by monoclonal antibody to alpha 4 beta 1 and to vascular cell adhesion molecule-1 (VCAM-1), a ligand for alpha 4 beta 1. VCAM-1 was found to be expressed by bone marrow stromal elements in vitro both constitutively at low level and at high levels after treatment with cytokines. Induction of VCAM-1 was cytokine- and time- dependent with maximum levels being obtained after 4 hours of exposure to a combination of interleukin-4 and tumor necrosis factor-alpha. Cytokine-induced stromal cells bound threefold higher numbers of CFU-GM and BFU-E, this increase being abrogated by anti-alpha 4 beta 1 and anti-VCAM-1 antibodies. In addition, the adhesion to stroma of more immature progenitors, the long-term culture initiating cells, also occurred through an alpha 4 beta 1/VCAM-1-dependent mechanism. These studies identify an adhesion mechanism of potential importance in the localization of primitive progenitors within the hematopoietic microenvironment.

scholarly journals Adhesion receptors on bone marrow stromal cells: in vivo expression of vascular cell adhesion molecule-1 by reticular cells and sinusoidal endothelium in normal and gamma-irradiated mice

Blood ◽  
1996 ◽  
Vol 87 (1) ◽  
pp. 73-82 ◽  
Author(s):  
K Jacobsen ◽  
J Kravitz ◽  
PW Kincade ◽  
DG Osmond
Keyword(s):  
Bone Marrow ◽  
Endothelial Cells ◽  
Cell Adhesion ◽  
Cell Adhesion Molecule ◽  
Vascular Cell Adhesion ◽  
Vascular Cell ◽  
Sinusoidal Endothelium ◽  
Reticular Cells ◽  
Cell Adhesion Molecule 1

Cell adhesion molecules (CAMs) play a key role in interactions between stromal and hematopoietic cells in bone marrow (BM) and in cell traffic through vascular endothelium. To examine the identity of CAMs involved in these processes in mouse BM, we have investigated the in vivo expression of vascular cell adhesion molecule-1 (VCAM-1) and its counter-receptor, very late antigen-4 (VLA-4). Radioiodinated monoclonal antibodies (MoAbs) detecting VLA-4 and VCAM-1 were injected intravenously. Antibody binding was detected in BM by light and electron microscope radioautography. VCAM-1 labeling was restricted to stromal reticular cells and endothelial cells lining BM sinusoids. VCAM- 1+ reticular cells formed patchy concentrations, especially in subosteal regions, associated with lymphoid, granulocytic, and erythroid cells. After gamma-irradiation to deplete hematopoietic cells, reticular cells and endothelial cells all showed VCAM-1 labeling in apparently increased intensity. VLA-4 labeling was shown by undifferentiated blast cells and lymphohematopoietic cells both in BM cell suspensions and in vivo, especially at reticular cell contact points. The results demonstrate that VCAM-1 is expressed in vivo by certain BM reticular cells, suggesting that the molecule mediates adhesion to multiple lineages of lymphohematopoietic cells. The finding that VCAM-1 is also expressed constitutively by BM sinusoidal endothelium, unlike its inductive expression by endothelia elsewhere, suggests that VCAM-1 and VLA-4 may be involved in regulating the normal cell traffic between BM and the blood stream.

Sign in / Sign up

Export Citation Format

Share Document