| First Author | Lananna BV | Year | 2018 |
| Journal | Cell Rep | Volume | 25 |
| Issue | 1 | Pages | 1-9.e5 |
| PubMed ID | 30282019 | Mgi Jnum | J:270346 |
| Mgi Id | MGI:6276087 | Doi | 10.1016/j.celrep.2018.09.015 |
| Citation | Lananna BV, et al. (2018) Cell-Autonomous Regulation of Astrocyte Activation by the Circadian Clock Protein BMAL1. Cell Rep 25(1):1-9.e5 |
| abstractText | Circadian clock dysfunction is a common symptom of aging and neurodegenerative diseases, though its impact on brain health is poorly understood. Astrocyte activation occurs in response to diverse insults and plays a critical role in brain health and disease. We report that the core circadian clock protein BMAL1 regulates astrogliosis in a synergistic manner via a cell-autonomous mechanism and a lesser non-cell-autonomous signal from neurons. Astrocyte-specific Bmal1 deletion induces astrocyte activation and inflammatory gene expression in vitro and in vivo, mediated in part by suppression of glutathione-S-transferase signaling. Functionally, loss of Bmal1 in astrocytes promotes neuronal death in vitro. Our results demonstrate that the core clock protein BMAL1 regulates astrocyte activation and function in vivo, elucidating a mechanism by which the circadian clock could influence many aspects of brain function and neurological disease. |
