Abstract
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.
Highlights
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by progressive memory loss and increasing dysfunction in mental behavior
We demonstrated that MiR-15bmediated pathogenesis of AD was through the pathways of Beta-site Amyloid precursor protein Cleaving Enzyme 1 (BACE1)
The results revealed that miR-15b expression levels were significantly lower in sporadic AD brain tissues when compared with those in brain specimens from other subjects (Figure 1A; P < 0.01)
Summary
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by progressive memory loss and increasing dysfunction in mental behavior. Progress has been made in identifying genes associated with AD, the pathogenesis of AD have not been elucidated until now. It has been revealed that miRNAs can affect various physiological and pathological processes including AD [4, 5]. Several miRNAs have been found to be related to AD pathogenesis by regulating the function of AD-relevant molecules [6, 7]. MiR-15b has been implicated as a mediator of apoptosis by targeting the antiapoptotic gene bcl in mesenchymal stem cells and rat hepatic cells [10]. We demonstrated that MiR-15bmediated pathogenesis of AD was through the pathways of BACE1
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