| First Author | Seo JY | Year | 2024 |
| Journal | iScience | Volume | 27 |
| Issue | 1 | Pages | 108617 |
| PubMed ID | 38188509 | Mgi Jnum | J:350880 |
| Mgi Id | MGI:7573738 | Doi | 10.1016/j.isci.2023.108617 |
| Citation | Seo JY, et al. (2024) TRPC4 deletion elicits behavioral defects in sociability by dysregulating expression of microRNA-138-2. iScience 27(1):108617 |
| abstractText | To investigate whether the defects in transient receptor potential canonical 4 (TRPC4), which is strongly expressed in the hippocampus, are implicated in ASD, we examined the social behaviors of mice in which Trpc4 was deleted (Trpc4(-/-)). Trpc4(-/-) mice displayed the core symptoms of ASD, namely, social disability and repetitive behaviors. In microarray analysis of the hippocampus, microRNA (miR)-138-2, the precursor of miR-138, was upregulated in Trpc4(-/-) mice. We also found that binding of Matrin3 (MATR3), a selective miR-138-2 binding nuclear protein, to miR-138-2 was prominently enhanced, resulting in the downregulation of miR-138 in Trpc4(-/-) mice. Some parameters of the social defects and repetitive behaviors in the Trpc4(-/-) mice were rescued by increased miR-138 levels following miR-138-2 infusion in the hippocampus. Together, these results suggest that Trpc4 regulates some signaling components that oppose the development of social behavioral deficits through miR-138 and provide a potential therapeutic strategy for ASD. |
