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MiR-340 Reduces the Accumulation of Amyloid-β Through Targeting BACE1 (β-site Amyloid Precursor Protein Cleaving Enzyme 1) in Alzheimer's Disease.
Curr Neurovasc Res. 2020; 17(1):86-92.CN

Abstract

BACKGROUND

Alzheimer's disease (AD) is the most common neurodegenerative disease, and the accumulation of amyloid-β is the initial process in AD. MicroRNAs (miRNAs) are widely known as key regulators of the accumulation of amyloid-β in AD. This study analyzed the potential effects and possible internal mechanisms of miR-340 on AD.

METHODS

The expression of miR-340 in senescence-accelerated mouse prone-8 (SAMP8) mouse and senescence-accelerated mice/resistant-1 (SAMR1) mouse was evaluated by qRT-PCR (quantitative real-time polymerase chain reaction). The expression of β-site amyloid precursor protein cleaving enzyme 1 (BACE1) was determined by qRT-PCR and western blot. The binding ability between miR-340 and BACE1 was verified by dual-luciferase reporter assay. In vitro cell model of AD was established in human neuroblastoma SH-SY5Y cells transfected with Swedish mutant form of amyloid precursor protein (APPswe). The effect of miR-340 on the accumulation of amyloid- β was investigated by western blot analysis. Flow cytometry was conducted to detect cell apoptosis.

RESULTS

MiR-340 was down-regulated in the hippocampus of AD model SAMP8 mouse compared to SAMR1 mouse, while BACE1 was up-regulated in SAMP8, suggesting a negative correlation between miR-340 and BACE1 in SAMP8 mouse. MiR-340 could directly bind with BACE1, and over-expression of miR-340 decreased expression of BACE1 in SH-SY5Y/APPswe cells. MiR- 340 reduced the accumulation of amyloid-β and suppressed cell apoptosis through targeting BACE1 in SH-SY5Y/APPswe cells.

CONCLUSION

MiR-340 was downregulated in AD and reduced the accumulation of amyloid-β through targeting BACE1, suggesting a potential therapeutic target for AD.

Links

Publisher Full Text (DOI)

Authors+Show Affiliations

Tan X
Department of Neurology, Jingzhou First People's Hospital, The First Affiliated Hospital of Yangtze University, Jingzhou City, Hubei Province, 434000, China.
Luo Y
Department of Neurology, Jingzhou First People's Hospital, The First Affiliated Hospital of Yangtze University, Jingzhou City, Hubei Province, 434000, China.
Pi D
Department of Neurology, Jingzhou First People's Hospital, The First Affiliated Hospital of Yangtze University, Jingzhou City, Hubei Province, 434000, China.
Xia L
Department of Neurology, Jingzhou First People's Hospital, The First Affiliated Hospital of Yangtze University, Jingzhou City, Hubei Province, 434000, China.
Li Z
Department of Neurology, Jingzhou First People's Hospital, The First Affiliated Hospital of Yangtze University, Jingzhou City, Hubei Province, 434000, China.
Tu Q
Department of Neurology, Jingzhou First People's Hospital, The First Affiliated Hospital of Yangtze University, Jingzhou City, Hubei Province, 434000, China.

MeSH

Alzheimer DiseaseAmyloid Precursor Protein SecretasesAmyloid beta-PeptidesAnimalsAspartic Acid EndopeptidasesCell LineCell Line, TumorDisease Models, AnimalDown-RegulationHippocampusHumansMiceMicroRNAsNeurons

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31957613

Citation

Tan, Xianpei, et al. "MiR-340 Reduces the Accumulation of Amyloid-β Through Targeting BACE1 (β-site Amyloid Precursor Protein Cleaving Enzyme 1) in Alzheimer's Disease." Current Neurovascular Research, vol. 17, no. 1, 2020, pp. 86-92.
Tan X, Luo Y, Pi D, et al. MiR-340 Reduces the Accumulation of Amyloid-β Through Targeting BACE1 (β-site Amyloid Precursor Protein Cleaving Enzyme 1) in Alzheimer's Disease. Curr Neurovasc Res. 2020;17(1):86-92.
Tan, X., Luo, Y., Pi, D., Xia, L., Li, Z., & Tu, Q. (2020). MiR-340 Reduces the Accumulation of Amyloid-β Through Targeting BACE1 (β-site Amyloid Precursor Protein Cleaving Enzyme 1) in Alzheimer's Disease. Current Neurovascular Research, 17(1), 86-92. https://doi.org/10.2174/1567202617666200117103931
Tan X, et al. MiR-340 Reduces the Accumulation of Amyloid-β Through Targeting BACE1 (β-site Amyloid Precursor Protein Cleaving Enzyme 1) in Alzheimer's Disease. Curr Neurovasc Res. 2020;17(1):86-92. PubMed PMID: 31957613.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - MiR-340 Reduces the Accumulation of Amyloid-β Through Targeting BACE1 (β-site Amyloid Precursor Protein Cleaving Enzyme 1) in Alzheimer's Disease. AU - Tan,Xianpei, AU - Luo,Yi, AU - Pi,Dingfang, AU - Xia,Liexin, AU - Li,Zhilian, AU - Tu,Qiang, PY - 2019/11/13/received PY - 2019/11/22/revised PY - 2019/11/24/accepted PY - 2020/1/21/pubmed PY - 2021/7/24/medline PY - 2020/1/21/entrez KW - Alzheimer's disease KW - BACE1 KW - amyloid precursor protein (APPswe) KW - amyloid-β KW - miR-340 KW - neuronal cell. SP - 86 EP - 92 JF - Current neurovascular research JO - Curr Neurovasc Res VL - 17 IS - 1 N2 - BACKGROUND: Alzheimer's disease (AD) is the most common neurodegenerative disease, and the accumulation of amyloid-β is the initial process in AD. MicroRNAs (miRNAs) are widely known as key regulators of the accumulation of amyloid-β in AD. This study analyzed the potential effects and possible internal mechanisms of miR-340 on AD. METHODS: The expression of miR-340 in senescence-accelerated mouse prone-8 (SAMP8) mouse and senescence-accelerated mice/resistant-1 (SAMR1) mouse was evaluated by qRT-PCR (quantitative real-time polymerase chain reaction). The expression of β-site amyloid precursor protein cleaving enzyme 1 (BACE1) was determined by qRT-PCR and western blot. The binding ability between miR-340 and BACE1 was verified by dual-luciferase reporter assay. In vitro cell model of AD was established in human neuroblastoma SH-SY5Y cells transfected with Swedish mutant form of amyloid precursor protein (APPswe). The effect of miR-340 on the accumulation of amyloid- β was investigated by western blot analysis. Flow cytometry was conducted to detect cell apoptosis. RESULTS: MiR-340 was down-regulated in the hippocampus of AD model SAMP8 mouse compared to SAMR1 mouse, while BACE1 was up-regulated in SAMP8, suggesting a negative correlation between miR-340 and BACE1 in SAMP8 mouse. MiR-340 could directly bind with BACE1, and over-expression of miR-340 decreased expression of BACE1 in SH-SY5Y/APPswe cells. MiR- 340 reduced the accumulation of amyloid-β and suppressed cell apoptosis through targeting BACE1 in SH-SY5Y/APPswe cells. CONCLUSION: MiR-340 was downregulated in AD and reduced the accumulation of amyloid-β through targeting BACE1, suggesting a potential therapeutic target for AD. SN - 1875-5739 UR - https://www.unboundmedicine.com/medline/citation/31957613/MiR_340_Reduces_the_Accumulation_of_Amyloid_β_Through_Targeting_BACE1__β_site_Amyloid_Precursor_Protein_Cleaving_Enzyme_1__in_Alzheimer's_Disease_ DB - PRIME DP - Unbound Medicine ER -