| First Author | Zhang Y | Year | 2014 |
| Journal | Int J Biol Sci | Volume | 10 |
| Issue | 9 | Pages | 1064-71 |
| PubMed ID | 25285038 | Mgi Jnum | J:226874 |
| Mgi Id | MGI:5698781 | Doi | 10.7150/ijbs.8415 |
| Citation | Zhang Y, et al. (2014) Deletion of Fgfr1 in osteoblasts enhances mobilization of EPCs into peripheral blood in a mouse endotoxemia model. Int J Biol Sci 10(9):1064-71 |
| abstractText | Endothelial progenitor cells (EPCs) contribute to neovascularization and vascular repair, and may exert a beneficial effect on the clinical outcome of sepsis. Osteoblasts act as a component of "niche" in bone marrow, which provides a nest for stem/progenitor cells and are involved in the formation and maintenance of stem/progenitor cells. Fibroblast growth factor receptor 1 (FGFR1) can regulate osteoblast activity and influence bone mass. So we explored the role of FGFR1 in EPC mobilization. Male mice with osteoblast-specific knockout of Fgfr1 (Fgfr1(fl/fl);OC-Cre) and its wild-type littermates (Fgfr1(fl/fl) ) were used in this study. Mice intraperitoneally injected with lipopolysaccharide (LPS) were used to measure the number of circulating EPCs in peripheral blood and serum stromal cell-derived factor 1alpha (SDF-1alpha). The circulating EPC number and the serum level of SDF-1alpha were significantly higher in Fgfr1(fl/fl);OC-Cre mice than those in Fgfr1(fl/fl) mice after LPS injection. In cell culture system, SDF-1alpha level was also significantly higher in Fgfr1(fl/fl);OC-Cre osteoblasts compared with that in Fgfr1(fl/fl) osteoblasts after LPS treatment. TRAP staining showed that there was no significant difference between the osteoclast activity of septic Fgfr1(fl/fl) and Fgfr1(fl/fl);OC-Cre mice. This study suggests that targeted deletion of Fgfr1 in osteoblasts enhances mobilization of EPCs into peripheral blood through up-regulating SDF-1alpha secretion from osteoblasts. |
