miR-15b represses BACE1 expression in sporadic Alzheimer’s disease
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Guohua Gong1,2,3,*, Fengmao An1,2,*, Yu Wang1,2, Ming Bian1,2, Li-Jun Yu1,2 and Chengxi Wei1,2
1Medicinal Chemistry and Pharmacology Institute, Inner Mongolia University for The Nationalities, Tongliao, Inner Mongolia, P.R. China
2Inner Mongolia Key Laboratory of Mongolian Medicine Pharmacology for Cardio-Cerebral Vascular System, Tongliao, Inner Mongolia, P.R. China
3First Clinical Medical of Inner Mongolia University for Nationalities, Tongliao, Inner Mongolia, P.R. China
*These authors have contributed equally to this work
Chengxi Wei, email: firstname.lastname@example.org
Li-Jun Yu, email: email@example.com
Keywords: alzheimer’s disease, miR-15b, BACE1, cell viability, cell apoptosis
Received: June 01, 2017 Accepted: August 06, 2017 Published: September 21, 2017
Beta-site Amyloid precursor protein Cleaving Enzyme 1 (BACE1) is conceived as a potential target for therapies against Alzheimer disease (AD). MicroRNAs (miRNAs) are small non-coding RNAs that negatively regulate gene expression in a sequence-specific manner. Although miRNAs have been increasingly recognized as important modulators in sporadic AD. In order to confirm whether miR-15b correlates with the BACE1 upregulation in sporadic AD, we firstly evaluated the expression of miR-15b and BACE1 in sporadic AD brain tissues and analyzed the correlation of miR-15b with BACE1. Then we determined the regulation of miR-15b in SH-SY5Y cells on the BACE1 expression. And finally we determined the targeting to 3’ UTR of BACE1 by miR-15b by a luciferase reporter. Downregulation of miR-15b alleviated Aβ-induced viability inhibition and decreased apoptosis in SH-SY5Y cells. Our results demonstrated that miR-15b play an important role in the cellular AD phenotype and might be involved in the pathogenesis of AD.
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