| First Author | Wang J | Year | 2018 |
| Journal | Free Radic Biol Med | Volume | 123 |
| Pages | 62-71 | PubMed ID | 29782989 |
| Mgi Jnum | J:355594 | Mgi Id | MGI:7750982 |
| Doi | 10.1016/j.freeradbiomed.2018.05.069 | Citation | Wang J, et al. (2018) NADPH oxidase 2 deletion enhances neurogenesis following traumatic brain injury. Free Radic Biol Med 123:62-71 |
| abstractText | The NADPH oxidase (NOX) enzyme family is a major source of reactive oxygen species (ROS) and contributor to the secondary pathology underlying traumatic brain injury (TBI). However, little is known about how NOX-derived ROS influences the proliferation and cell-fate determination of neural stem/progenitor cells (NSCs/NPCs) following TBI. In the current study, we found that deletion of NOX2 (NOX2-KO) significantly decreases the population of radial glia-like NSCs and neuroblasts but maintains the population of non-radial Sox2 expressing stem cells under physiological (non-injury) conditions. Surprisingly, the brains of NOX2-KO mice demonstrated a robust increase in the number of neuroblasts during the first week after TBI, as compared to the wild-type group. This increase may result from an enhanced proliferation of NPCs in a lower ROS environment after brain injury, as further examination revealed a significant increase of dividing neuroblasts in both NOX2-KO and NOX inhibitor-treated mouse brain during the first week following TBI. Finally, 5-Bromo-2'-deoxyuridine (BrdU) lineage tracing demonstrated a significantly increased number of newborn neurons were present in the perilesional cortex of NOX2-KO mice at 5 weeks post TBI, indicating that deletion of NOX2 promotes long-term neurogenesis in the injured brain following TBI. Altogether, these findings suggest that targeting NOX through genetic deletion or inhibition enhances post-injury neurogenesis, which may be beneficial for recovery following TBI. |
