| First Author | Evrard S | Year | 2011 |
| Journal | Blood | Volume | 117 |
| Issue | 1 | Pages | 246-9 |
| PubMed ID | 20944070 | Mgi Jnum | J:168424 |
| Mgi Id | MGI:4888186 | Doi | 10.1182/blood-2010-07-294447 |
| Citation | Evrard S, et al. (2011) Thrombospondin-1 is not the major activator of TGF-beta1 in thrombopoietin-induced myelofibrosis. Blood 117(1):246-9 |
| abstractText | Transforming growth factor-beta1 (TGF-beta1) is the most important cytokine involved in the promotion of myelofibrosis. Mechanisms leading to its local activation in the bone marrow environment remain unclear. As a recent study has highlighted the role of thrombospondin-1 (TSP-1) in platelet-derived TGF-beta1 activation, we investigated the role of TSP-1 in the TPO(high) murine model of myelofibrosis. Two groups of engrafted mice, WT TPO(high) and Tsp-1-null TPO(high), were constituted. All mice developed a similar myeloproliferative syndrome and an increase in total TGF-beta1 levels in the plasma and in extracellular fluids of marrow and spleen. Surprisingly, we were able to detect the active form of TGF-beta1 in Tsp-1-null TPO(high) mice. Accordingly, these mice developed marrow and spleen fibrosis, with intriguingly a higher grade than in WT TPO(high) mice. Our results show that TSP-1 is not the major activator of TGF-beta1 in TPO-induced myelofibrosis, suggesting the contribution of another mechanism in the megakaryocyte/platelet compartment. |
