Tags

Type your tag names separated by a space and hit enter

MicroRNA-384 regulates both amyloid precursor protein and β-secretase expression and is a potential biomarker for Alzheimer's disease.
Int J Mol Med 2014; 34(1):160-6IJ

Abstract

Amyloid precursor protein (APP) and β-site APP cleaving enzyme (BACE-1) play important roles in the pathogenesis of Alzheimer's disease (AD). In this study, using bioinformatics analysis, we demonstrate that miR-384 is a microRNA (miRNA or miR) predicted to potentially target the 3' untranslated regions (3'-UTRs) of both APP and BACE-1. SH-SY5Y cells were transfected with miR-384 mimic oligonucleotide, miR-384 inhibitor oligonucleotide, or a non-specific control siRNA. We found that the overexpression of miR-384 suppressed the mRNA and protein expression of both APP and BACE-1. The miR-384 inhibitor oligonucleotide induced the upregulation of APP and BACE-1. The activity of BACE-1 was altered following the change in its protein expression. The binding sites of miR-384 on the 3'-UTRs of APP and BACE-1 were identified by luciferase assay. Furthermore, cells were treasted with amyloid-β (Aβ)42. Aβ42 downregulated miR-384 expression, leading to the continuous reduction in miR-384 expression. In addition, using a mouse model of AD, as well as patients with mild cognitive impairment (MCI) and dementia of Alzheimer's type (DAT), we examined the levels of miR-384 in cerebral spinal fluid (CSF) and serum. Patients with MCI and DAT had lower blood miR-384 levels compared with the controls. In addition, patients with DAT had lower blood miR-384 levels in blood compared with the MCI group. We also found decreased miR-384 expression in the several cerebral spinal fluid (CSF) of the patients with DAT. Negative correlations were observed between miR-384 and Aβ42 in the serum and CSF from patients with AD. In conclusion, these findings demonstrate that miR-384 may plays a role in the development of AD and may be a potential non-invasive biomarker for the diagnosis of AD.

Authors+Show Affiliations

Clinical Laboratory of Xuanwu Hospital, Capital Medical University, Beijing 100053, P.R. China.Clinical Laboratory of Xuanwu Hospital, Capital Medical University, Beijing 100053, P.R. China.Clinical Laboratory of Xuanwu Hospital, Capital Medical University, Beijing 100053, P.R. China.Clinical Laboratory of Xuanwu Hospital, Capital Medical University, Beijing 100053, P.R. China.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24827165

Citation

Liu, Chen-Geng, et al. "MicroRNA-384 Regulates Both Amyloid Precursor Protein and Β-secretase Expression and Is a Potential Biomarker for Alzheimer's Disease." International Journal of Molecular Medicine, vol. 34, no. 1, 2014, pp. 160-6.
Liu CG, Wang JL, Li L, et al. MicroRNA-384 regulates both amyloid precursor protein and β-secretase expression and is a potential biomarker for Alzheimer's disease. Int J Mol Med. 2014;34(1):160-6.
Liu, C. G., Wang, J. L., Li, L., & Wang, P. C. (2014). MicroRNA-384 regulates both amyloid precursor protein and β-secretase expression and is a potential biomarker for Alzheimer's disease. International Journal of Molecular Medicine, 34(1), pp. 160-6. doi:10.3892/ijmm.2014.1780.
Liu CG, et al. MicroRNA-384 Regulates Both Amyloid Precursor Protein and Β-secretase Expression and Is a Potential Biomarker for Alzheimer's Disease. Int J Mol Med. 2014;34(1):160-6. PubMed PMID: 24827165.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - MicroRNA-384 regulates both amyloid precursor protein and β-secretase expression and is a potential biomarker for Alzheimer's disease. AU - Liu,Chen-Geng, AU - Wang,Jin-Ling, AU - Li,Lei, AU - Wang,Pei-Chang, Y1 - 2014/05/13/ PY - 2014/01/05/received PY - 2014/05/08/accepted PY - 2014/5/16/entrez PY - 2014/5/16/pubmed PY - 2014/12/31/medline SP - 160 EP - 6 JF - International journal of molecular medicine JO - Int. J. Mol. Med. VL - 34 IS - 1 N2 - Amyloid precursor protein (APP) and β-site APP cleaving enzyme (BACE-1) play important roles in the pathogenesis of Alzheimer's disease (AD). In this study, using bioinformatics analysis, we demonstrate that miR-384 is a microRNA (miRNA or miR) predicted to potentially target the 3' untranslated regions (3'-UTRs) of both APP and BACE-1. SH-SY5Y cells were transfected with miR-384 mimic oligonucleotide, miR-384 inhibitor oligonucleotide, or a non-specific control siRNA. We found that the overexpression of miR-384 suppressed the mRNA and protein expression of both APP and BACE-1. The miR-384 inhibitor oligonucleotide induced the upregulation of APP and BACE-1. The activity of BACE-1 was altered following the change in its protein expression. The binding sites of miR-384 on the 3'-UTRs of APP and BACE-1 were identified by luciferase assay. Furthermore, cells were treasted with amyloid-β (Aβ)42. Aβ42 downregulated miR-384 expression, leading to the continuous reduction in miR-384 expression. In addition, using a mouse model of AD, as well as patients with mild cognitive impairment (MCI) and dementia of Alzheimer's type (DAT), we examined the levels of miR-384 in cerebral spinal fluid (CSF) and serum. Patients with MCI and DAT had lower blood miR-384 levels compared with the controls. In addition, patients with DAT had lower blood miR-384 levels in blood compared with the MCI group. We also found decreased miR-384 expression in the several cerebral spinal fluid (CSF) of the patients with DAT. Negative correlations were observed between miR-384 and Aβ42 in the serum and CSF from patients with AD. In conclusion, these findings demonstrate that miR-384 may plays a role in the development of AD and may be a potential non-invasive biomarker for the diagnosis of AD. SN - 1791-244X UR - https://www.unboundmedicine.com/medline/citation/24827165/MicroRNA_384_regulates_both_amyloid_precursor_protein_and_β_secretase_expression_and_is_a_potential_biomarker_for_Alzheimer's_disease_ L2 - http://www.spandidos-publications.com/ijmm/34/1/160 DB - PRIME DP - Unbound Medicine ER -