| First Author | Guo Y | Year | 2013 |
| Journal | Lab Invest | Volume | 93 |
| Issue | 7 | Pages | 825-33 |
| PubMed ID | 23711824 | Mgi Jnum | J:198732 |
| Mgi Id | MGI:5499057 | Doi | 10.1038/labinvest.2013.73 |
| Citation | Guo Y, et al. (2013) The modest impact of transcription factor Nrf2 on the course of disease in an ALS animal model. Lab Invest 93(7):825-33 |
| abstractText | Oxidative stress is associated with the pathogenesis of amyotrophic lateral sclerosis (ALS). Nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway is one of the major cellular defense mechanisms against oxidative stress. However, the role of Nrf2-mediated neuroprotection (antioxidant defense) in the disease development of ALS remains unclear. To further investigate the role of Nrf2 in ALS, we genetically eliminate the Nrf2 gene from SOD1-G93A mice, a commonly used ALS mouse model, by generating a double mutant (Nrf2-/- SOD1-G93A mice). We found that it only had a modest impact on the course of disease by knocking out Nrf2 gene in these mice. Further studies demonstrated that, among previously known Nrf2-regulated phase II enzymes, only NAD(P)H: quinone oxidoreductase 1 induction was significantly affected by the elimination of Nrf2 gene in SOD1-G93A mice. Taken together, our data suggested that Nrf2 is not the sole mediator for the induction of antioxidant genes in SOD1-G93A mice, and Nrf2-mediated neuroprotection is not the key protective mechanism against neurodegeneration in those mice. |
