| First Author | Fontaine V | Year | 2006 |
| Journal | Am J Pathol | Volume | 169 |
| Issue | 5 | Pages | 1855-62 |
| PubMed ID | 17071606 | Mgi Jnum | J:114567 |
| Mgi Id | MGI:3689447 | Doi | 10.2353/ajpath.2006.060260 |
| Citation | Fontaine V, et al. (2006) Essential role of bone marrow fibroblast growth factor-2 in the effect of estradiol on reendothelialization and endothelial progenitor cell mobilization. Am J Pathol 169(5):1855-62 |
| abstractText | 17beta-Estradiol (E(2)) accelerates reendothelialization and increases the number of circulating endothelial progenitor cells (EPCs), but whether fibroblast growth factor-2 (FGF2) is involved in these processes remains unknown. Here we explored the role of FGF2 in the effect of E(2) on reendothelialization and EPC levels in a mouse model. As previously reported, E(2) increased both the velocity of reendothelialization and the number of circulating EPCs in ovariectomized wild-type (Fgf2(+/+)) mice. In contrast, the effect of E(2) on both parameters was abolished in FGF2-deficient mice (Fgf2(-/-)), demonstrating that FGF2 is absolutely required for these effects of E(2). To test the implication of medullary and extramedullary FGF2, we developed chimeric mice by grafting Fgf2(-/-) bone marrow to Fgf2(+/+) [Fgf2(-/-) bone marrow (BM) = >Fgf2(+/+)] mice and observed that the effect of E(2) on both reendothelialization and EPC levels was abolished. In contrast, both effects of E(2) in Fgf2(+/+)BM = >Fgf2(-/-) mice were similar to those observed in Fgf2(+/+) mice, demonstrating that only BM-derived, but not extramedullary, FGF2 is required for both effects. Interestingly, E(2) was found to markedly increase both FGF2(lmw) and FGF2(hmw) in bone marrow. In conclusion, FGF2, specifically medullary FGF2, is necessary and sufficient to mediate the accelerative effect of E(2) on both reendothelialization and EPC mobilization. |
