| First Author | Zhou Z | Year | 2019 |
| Journal | Cell Signal | Volume | 63 |
| Pages | 109378 | PubMed ID | 31369826 |
| Mgi Jnum | J:294684 | Mgi Id | MGI:6457183 |
| Doi | 10.1016/j.cellsig.2019.109378 | Citation | Zhou Z, et al. (2019) Deletion of HO-1 blocks development of B lymphocytes in mice. Cell Signal 63:109378 |
| abstractText | B lymphocytes, a key cluster of cells composing the immune system, can protect against abnormal biological factors. Heme oxygenase-1 (HO-1) plays important roles in cell proliferation and immune regulation, but its effects on the development and growth of B lymphocytes are still unknown. Herein, the count of B lymphocytes in HO-1 gene knockout (HO-1(+/-)) mice was significantly lower than that of the HO-1 gene wild-type (HO-1(WT)) mice. Meanwhile, the cell count of HO-1(+/-) mice did not recover after irradiation for one week, due to the G0/G1 phase arrest of Pro-B cells and the augmented apoptosis of Pre-B cells. Up-regulation of HO-1 by lentivirus attenuated the Pro-B cell cycle arrest and Pre-B cell apoptosis. To understand the molecular mechanism by which HO-1 knockout blocked B lymphocyte development, protein-to-protein interaction network and Western blot were used. The PI3K/AKT signaling pathway mediated the regulatory effects of HO-1 on B lymphocytes. In conclusion, HO-1 is a crucial transcriptional repressor for B cell development. |
