期刊
CELL REPORTS
卷 15, 期 5, 页码 1024-1036出版社
CELL PRESS
DOI: 10.1016/j.celrep.2016.03.090
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资金
- Brain and Behavior Research Foundation
- NIH [R01 MH101454, R01 MH106056, R01 MH097276, R01 GM114472]
- New York Stem Cell Foundation
- Health Research Board Clinical Scientist Award
- Lundbeck Foundation [R155-2014-1724] Funding Source: researchfish
Converging evidence indicates that microRNAs (miRNAs) may contribute to disease risk for schizophrenia (SZ). We show that microRNA-9 (miR-9) is abundantly expressed in control neural progenitor cells (NPCs) but also significantly downregulated in a subset of SZ NPCs. We observed a strong correlation between miR-9 expression and miR-9 regulatory activity in NPCs as well as between miR-9 levels/activity, neural migration, and diagnosis. Overexpression of miR-9 was sufficient to ameliorate a previously reported neural migration deficit in SZ NPCs, whereas knockdown partially phenocopied aberrant migration in control NPCs. Unexpectedly, proteomic- and RNA sequencing (RNA-seq)-based analysis revealed that these effects were mediated primarily by small changes in expression of indirect miR-9 targets rather than large changes in direct miR-9 targets; these indirect targets are enriched for migration-associated genes. Together, these data indicate that aberrant levels and activity of miR-9 may be one of the many factors that contribute to SZ risk, at least in a subset of patients.
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