MicroRNA-29c targets β-site amyloid precursor protein-cleaving enzyme 1 and has a neuroprotective role in vitro and in vivo

Yang,Guoshuai; Song,Yanmin; Zhou,Xiaoyan; Deng,Yidong; Liu,Tao; Weng,Guohu; Yu,Dan; Pan,Suyue

doi:10.3892/mmr.2015.3728

MicroRNA-29c targets β-site amyloid precursor protein-cleaving enzyme 1 and has a neuroprotective role in vitro and in vivo

Authors:
- Guoshuai Yang
- Yanmin Song
- Xiaoyan Zhou
- Yidong Deng
- Tao Liu
- Guohu Weng
- Dan Yu
- Suyue Pan
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Affiliations: Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China, Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China, Department of Neurology, Haikou People's Hospital, Haikou, Hainan 570208, P.R. China
Published online on: May 5, 2015 https://doi.org/10.3892/mmr.2015.3728
Pages: 3081-3088

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Abstract

Alzheimer's disease (AD), characterized by β-amyloid deposition and neurodegeneration, is the most common cause of dementia worldwide. Emerging evidence suggests that ectopic expression of micro (mi)RNAs is involved in the pathogenesis of AD. There is increasing evidence that miRNAs expressed in the brain are involved in neuronal development, survival and apoptosis. The expression of β‑site amyloid precursor protein‑cleaving enzyme 1 (BACE1) is regulated by dysregulated miRNAs in the brain. The present study determined the expression levels of the miRNA‑29 (miR‑29) family in peripheral blood samples of patients with AD and demonstrated a marked decrease in the expression of miR‑29c compared with age‑matched controls. In addition, a significant increase in the exprssion of BACE1 was observed in the peripheral blood of patients with AD. Correlation analysis revealed that the expression of miR‑29c was negatively correlated with the protein expression of BACE1 in the peripheral blood samples from patients with AD. The present study also investigated the role of miR‑29 on hippocampal neurons in vitro and in vivo. The results demonstrated that the upregulation of miR‑29c promoted learning and memory behaviors in SAMP8 mice, at least partially, by increasing the activity of protein kinase A/cAMP response element‑binding protein, involved in neuroprotection. This evidence suggested that miR‑29c may be a promising potential therapeutic target against AD.

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