| First Author | Qing Y | Year | 2014 |
| Journal | Blood | Volume | 123 |
| Issue | 7 | Pages | 1002-11 |
| PubMed ID | 24394664 | Mgi Jnum | J:208689 |
| Mgi Id | MGI:5564833 | Doi | 10.1182/blood-2013-08-521716 |
| Citation | Qing Y, et al. (2014) Bcl2 overexpression rescues the hematopoietic stem cell defects in Ku70-deficient mice by restoration of quiescence. Blood 123(7):1002-11 |
| abstractText | DNA repair is essential for hematopoietic stem cell (HSC) maintenance. Ku70 is a key component of the nonhomologous end-joining pathway, which is the major pathway for DNA double-strand break repair. We find that HSCs from Ku70-deficient mice are severely defective in self-renewal, competitive repopulation, and bone marrow (BM) hematopoietic niche occupancy and that loss of quiescence results in a dramatic defect in the maintenance of Ku70-deficient HSCs. Interestingly, although overexpression of Bcl2 does not rescue the severe combined immunodeficiency phenotype in Ku70-deficient mice, overexpression of Bcl2 in Ku70-deficient HSCs almost completely rescued the impaired HSC quiescence, repopulation, and BM hematopoietic niche occupancy capacities. Together, our data indicate that the HSC maintenance defect of Ku70-deficient mice is due to the loss of HSC quiescent populations, whereas overexpression of Bcl2 rescues the HSC defect in Ku70-deficient mice by restoration of quiescence. Our study uncovers a novel role of Bcl2 in HSC quiescence regulation. |
