| First Author | Motoyama N | Year | 1999 |
| Journal | J Exp Med | Volume | 189 |
| Issue | 11 | Pages | 1691-8 |
| PubMed ID | 10359572 | Mgi Jnum | J:55961 |
| Mgi Id | MGI:1339826 | Doi | 10.1084/jem.189.11.1691 |
| Citation | Motoyama N, et al. (1999) bcl-x prevents apoptotic cell death of both primitive and definitive erythrocytes at the end of maturation. J Exp Med 189(11):1691-8 |
| abstractText | bcl-x is a member of the bcl-2 gene family, which regulates apoptotic cell death in various cell lineages. There is circumstantial evidence suggesting that bcl-x might play a role in the apoptosis of erythroid lineage cells, although there is no direct evidence. In this study, we used Bcl-X null mouse embryonic stem (ES) cells, and showed that Bcl-X is indispensable for the production of both embryonic primitive erythrocytes (EryP) and adult definitive erythrocytes (EryD) at the end of their maturation. In vivo, bcl-x-/- ES cells did not contribute to circulating EryD in adult chimeric mice that were produced by blastocyst microinjection of the bcl-x-/- ES cells. bcl-x-/- EryP and EryD were produced by in vitro differentiation induction of ES cells on macrophage colony-stimulating factor-deficient stromal cell line OP9, and further analysis was carried out. The emergence of immature EryP and EryD from bcl-x-/- ES cells was similar to that from bcl-x+/+ ES cells. However, prominent cell death of bcl-x-/- EryP and EryD occurred when the cells matured. The data show that the antiapoptotic function of bcl-x acts at the very end of erythroid maturation. |
