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Published on: December 26, 2015
miR-29c regulates NAV3 protein expression in a transgenic mouse model of Alzheimer's disease
Yuanyuan Zong1, Pin Yu2, Hongxia Cheng1
1Department of Pathology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, PR China.
Abstract:
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.
Insights
MicroRNA-29c (miR-29c) is linked to Alzheimer's disease (AD) pathogenesis. This study shows miR-29c directly downregulates NAV3 expression in young AD mouse brains, suggesting a role in neurodegeneration.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- The microRNA-29 family (miRNA-29s) is implicated in Alzheimer's disease (AD) pathogenesis.
- miRNA-29 family members show differential regulation and subcellular distribution across diseases.
Purpose of the Study:
- Investigate the differential expression of miR-29c in the hippocampus and frontal cortex of young APPswe/PSΔE9 AD mouse brains.
- Determine the relationship between miR-29c and neurone navigator 3 (NAV3) expression in the context of AD.
Main Methods:
- Differential expression analysis of miR-29c and NAV3 in AD mouse brain regions.
- In vitro experiments to assess miR-29c's direct effect on NAV3 protein levels.
- Bioinformatic analysis of the miR-29c binding site in the 3' UTR of mouse NAV3 mRNA.
Main Results:
- Observed inverse expression between miR-29c and NAV3 in the hippocampus and frontal cortex of young AD mice.
- Demonstrated that miR-29c directly downregulates NAV3 protein expression in vitro.
- Identified a functional miR-29c binding site within the 3' UTR of mouse NAV3 mRNA.
Conclusions:
- miR-29c directly mediates the downregulation of NAV3 protein.
- These findings suggest a potential role for miR-29c in neurodegenerative processes, specifically in young AD mice, through the regulation of NAV3 expression.
