| First Author | Vergori L | Year | 2015 |
| Journal | Stem Cells | Volume | 33 |
| Issue | 4 | Pages | 1292-303 |
| PubMed ID | 25524540 | Mgi Jnum | J:223973 |
| Mgi Id | MGI:5660714 | Doi | 10.1002/stem.1924 |
| Citation | Vergori L, et al. (2015) PPARalpha regulates endothelial progenitor cell maturation and myeloid lineage differentiation through a NADPH oxidase-dependent mechanism in mice. Stem Cells 33(4):1292-303 |
| abstractText | Peroxisome proliferator-activated receptor-alpha (PPARalpha) is a key modulator of lipid metabolism. Here, we propose that PPARalpha regulates the maturation and function of bone marrow (BM) progenitor cells. Although PPARalpha deletion increased the number of BM-resident cells and the differentiation of endothelial progenitor cells (EPCs) and monocytic progenitor cells, it impaired re-endothelialization of injured carotid artery that was associated with reduced circulating EPCs. Also, PPARalpha deletion diminished the in vivo proangiogenic effect of PPARalpha agonist without affecting EPC differentiation markers. Macrophage colony-stimulating factor treatment increased the population of monocytic progenitor cells as well as secretome of BM-derived cells in PPARalpha wild-type but not in knockout mice. In addition, PPARalpha-null mice displayed reduced lymphocytes and increased monocytes and neutrophils in the blood. Furthermore, PPARalpha-null mice exhibited increments in the number of total cells (as well as of phenotypically distinct subpopulations of lymph node cells) but also a significant alteration in the number of various subpopulations of splenocytes and thymocytes. Finally, PPARalpha negatively regulated reactive oxygen species derived by NADPH oxidase in BM-resident progenitor cells. Taken together, our data provide evidence that PPARalpha is a critical regulator of recruitment, homing, and maturation of BM-derived progenitor cells. |
