| First Author | Fu Y | Year | 2022 |
| Journal | Cell Death Dis | Volume | 13 |
| Issue | 4 | Pages | 292 |
| PubMed ID | 35365601 | Mgi Jnum | J:323615 |
| Mgi Id | MGI:7263509 | Doi | 10.1038/s41419-022-04721-z |
| Citation | Fu Y, et al. (2022) Loss of neurodevelopmental-associated miR-592 impairs neurogenesis and causes social interaction deficits. Cell Death Dis 13(4):292 |
| abstractText | microRNA-592 (miR-592) has been linked to neurogenesis, but the influence of miR-592 knockout in vivo remains unknown. Here, we report that miR-592 knockout represses IPC-to-mature neuron transition, impairs motor coordination and reduces social interaction. Combining the RNA-seq and tandem mass tagging-based quantitative proteomics analysis (TMT protein quantification) and luciferase reporter assays, we identified MeCP2 as the direct targetgene of miR-592 in the mouse cortex. In Tg(MECP2) mice, lipofection of miR-592 efficiently reduced MECP2 expression in the brains of Tg(MECP2) mice at E14.5. Furthermore, treatment with miR-592 partially ameliorated the autism-like phenotypes observed in adult Tg(MECP2) mice. The findings demonstrate that miR-592 might play a novel role in treating the neurodevelopmental-associated disorder. |
