Transforming growth factor-β1 primes proliferating adult neural progenitor cells to electrophysiological functionality

Glia ◽  
2013 ◽  
Vol 61 (11) ◽  
pp. 1767-1783 ◽  
Author(s):  
Sabrina Kraus ◽  
Bernadette Lehner ◽  
Nadine Reichhart ◽  
Sebastien Couillard-Despres ◽  
Katrin Wagner ◽  
...  
Keyword(s):  
Growth Factor ◽  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Transforming Growth Factor ◽  
Neural Progenitor ◽  
Transforming Growth Factor Β1

Chemokine receptor CXCR4 signaling modulates the growth factor-induced cell cycle of self-renewing and multipotent neural progenitor cells

Glia ◽  
2010 ◽  
Vol 59 (1) ◽  
pp. 108-118 ◽  
Author(s):  
Meizhang Li ◽  
Cathleen J. Chang ◽  
Justin D. Lathia ◽  
Li Wang ◽  
Holly L. Pacenta ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Progenitor Cells ◽  
Chemokine Receptor ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
Cxcr4 Signaling ◽  
Chemokine Receptor Cxcr4

scholarly journals Transforming growth factor-β1 modulates responses of CD34+ cord blood cells to stromal cell-derived factor-1/CXCL12

Blood ◽  
2005 ◽  
Vol 106 (2) ◽  
pp. 485-493 ◽  
Author(s):  
Sunanda Basu ◽  
Hal E. Broxmeyer
Keyword(s):  
Bone Marrow ◽  
Growth Factor ◽  
Cord Blood ◽  
Progenitor Cells ◽  
Stromal Cell ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Cd34 Cells ◽  
Stromal Cell Derived Factor ◽  
Tgf Β1

Abstract Disruption of stromal cell-derived factor-1 (SDF-1/CXCL12 [CXC chemokine ligand 12]) interaction leads to mobilization of stem/progenitor cells from bone marrow to circulation. However, prolonged exposure of CD34+ cells to SDF-1 desensitizes them to SDF-1. So how do cells remain responsive to SDF-1 in vivo when they are continuously exposed to SDF-1? We hypothesized that one or more mechanisms mediated by cytokines exist that could modulate SDF-1 responsiveness of CD34+ cells and the desensitization process. We considered transforming growth factor-β1 (TGF-β1) a possible candidate, since TGF-β1 has effects on CD34+ cells and is produced by stromal cells, which provide niches for maintenance and proliferation of stem/progenitor cells. TGF-β1 significantly restored SDF-1–induced chemotaxis and sustained adhesion responses in cord blood CD34+ cells preexposed to SDF-1. Effects of TGF-β1 were dependent on the dose and duration of TGF-β1 pretreatment. Phosphorylation of extracellular signal-regulated kinase 1 (Erk1)/Erk2 was implicated in TGF-β1 modulation of migratory and adhesion responses to SDF-1. Our results indicate that low levels of TGF-β1 can modulate SDF-1 responsiveness of CD34+ cells and thus may facilitate SDF-1–mediated retention and nurturing of stem/progenitor cells in bone marrow.

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