| First Author | Dhahri D | Year | 2016 |
| Journal | Blood | Volume | 128 |
| Issue | 8 | Pages | 1063-75 |
| PubMed ID | 27283026 | Mgi Jnum | J:236265 |
| Mgi Id | MGI:5805603 | Doi | 10.1182/blood-2015-10-673103 |
| Citation | Dhahri D, et al. (2016) Fibrinolytic crosstalk with endothelial cells expands murine mesenchymal stromal cells. Blood 128(8):1063-75 |
| abstractText | Tissue plasminogen activator (tPA), aside from its vascular fibrinolytic action, exerts various effects within the body, ranging from synaptic plasticity to control of cell fate. Here, we observed that by activating plasminogen and matrix metalloproteinase-9, tPA expands murine bone marrow-derived CD45(-)TER119(-)Sca-1(+)PDGFRalpha(+) mesenchymal stromal cells (PalphaS-MSCs) in vivo through a crosstalk between PalphaS-MSCs and endothelial cells. Mechanistically, tPA induces the release of Kit ligand from PalphaS-MSCs, which activates c-Kit(+) endothelial cells to secrete MSC growth factors: platelet-derived growth factor-BB (PDGF-BB) and fibroblast growth factor 2 (FGF2). In synergy, FGF2 and PDGF-BB upregulate PDGFRalpha expression in PalphaS-MSCs, which ultimately leads to PalphaS-MSC expansion. These data show a novel mechanism by which the fibrinolytic system expands PalphaS-MSCs through a cytokine crosstalk between niche cells. |
