Research ReportmiR-29c regulates NAV3 protein expression in a transgenic mouse model of Alzheimer׳s disease

highlights
- Aberrent expression of miR-29c and NAV3 protein in different AD mice brain regions.
- miR-29c could directly regulate NAV3 protein expression in vitro.
- Binding site was slightly different from human NAV3 mRNA.

The microRNA-29 family (miRNA-29s) has three mature members, miR-29a, miR-29b and miR-29c, which have been implicated in the regulation of the pathogenesis of Alzheimer׳s disease (AD). The miR-29 family members exhibit differential regulation in various diseases and different subcellular distribution. In the present study, we initially investigated differential expression of miR-29c in the hippocampus and the frontal cortex of the young APPswe/PSΔE9 mouse brain, accompanied by inverse expression of neurone navigator 3 (NAV3), a regulator of axon guidance. We observed that miR-29c directly mediated downregulation of NAV3 protein expression in vitro. The mouse NAV3 mRNA has a functional miR-29c binding site in the 3′ UTR, which localized in the position between 830-836 bp of 3′UTR region, slightly different from human NAV3 mRNA binding site.These observations suggest that miR-29c may be involved in neurodegenerative processes by regulating NAV3 expression in the young AD mouse.