MicroRNA-16 targets amyloid precursor protein to potentially modulate Alzheimer's-associated pathogenesis in SAMP8 mice

Liu, Wei; Liu, Chang; Zhu, Jing-xi; Shu, Pengcheng; Yin, Bin; Gong, Yanhua; Qiang, Boqin; Yuan, Jing; Peng, Xiaozhong

doi:10.1016/j.neurobiolaging.2010.04.034

Cited by 164 publications

(116 citation statements)

References 47 publications

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“…Although many studies have been focused on miRNAs that regulate APP expression to Alzheimer's disease pathogenesis [22][23][24] , we identify one of the first miRNAs (miR-574-5p) that are regulated by APP. In addition, we further suggest the mechanism of how APP regulates the transcription of miR-574-5p via regulation of transcription level of Fam114a1, a gene which encoding miR-574-5p.…”

Section: Discussionmentioning

confidence: 99%

Amyloid precursor protein regulates neurogenesis by antagonizing miR-574-5p in the developing cerebral cortex

et al. 2014

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Amyloid precursor protein (APP) is a transmembrane glycoprotein proteolytically processed to release amyloid beta, a pathological hallmark of Alzheimer's disease. APP is expressed throughout the developing and mature brain; however, the primary function of this protein is unknown. We previously demonstrated that APP deficiency enhances neurogenesis, but the mechanisms underlying this process are not known. Here we show that APP regulates the expression of microRNAs in the cortex and in neural progenitors, specifically repressing miR-574-5p. We also show that overexpression of miR-574-5p promotes neurogenesis, but reduces the neural progenitor pool. In contrast, the reduced expression of miR-574-5p inhibits neurogenesis and stimulates proliferation in vitro and in utero. We further demonstrate that the inhibition of miR-574-5p in APP-knockout mice rescues the phenotypes associated with APP deficiency in neurogenesis. Taken together, these results reveal a mechanism in which APP regulates the neurogenesis through miRNA-mediated post-transcriptional regulation.

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Section: Discussionmentioning

confidence: 99%

Amyloid precursor protein regulates neurogenesis by antagonizing miR-574-5p in the developing cerebral cortex

et al. 2014

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“…Similarly, alterations of miRNA networks cause neurodegenerative disorders, including AD, Parkinson disease (21), and Huntington disease (22). Indeed, recent studies demonstrate that dysregulation of specific miRNAs contributes to amyloidogenesis in the pathogenesis of AD, but all such research has focused on the regulation of APP (23)(24)(25)(26)(27) or BACE1 (i.e. ␤-secretase and ␤-site APP cleaving enzyme 1) (28 -30).…”

Section: Alzheimer Disease (Ad)mentioning

confidence: 99%

MicroRNA-144 Is Regulated by Activator Protein-1 (AP-1) and Decreases Expression of Alzheimer Disease-related A Disintegrin and Metalloprotease 10 (ADAM10)

Cheng

Zhang

et al. 2013

Journal of Biological Chemistry

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Background: MicroRNA (miR) dysregulation is found in Alzheimer disease (AD). A disintegrin and metalloprotease 10 (ADAM10) prevents generation of amyloid ␤ (A␤) and decrease AD pathology. Results: miR-144 suppresses ADAM10 expression and is up-regulated by activator protein-1. Conclusion: miR-144 is a negative regulator of ADAM10 and may be involved in AD pathogenesis. Significance:The first work to demonstrate the function of miRNA-144 and its regulation in the pathogenesis of AD.

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“…We and others have begun to describe the contributions that miRNAs bring to the post-transcriptional control of gene products implicated in AD, including APP (42)(43)(44)(45)(46)(47)(48)(49)(50). Others have previously identified and partially characterized miRNAs that also appear to negatively regulate BACE1 expression (18,(51)(52)(53).…”

mentioning

confidence: 99%

MicroRNA-339-5p Down-regulates Protein Expression of β-Site Amyloid Precursor Protein-Cleaving Enzyme 1 (BACE1) in Human Primary Brain Cultures and Is Reduced in Brain Tissue Specimens of Alzheimer Disease Subjects

Long

Ray

Lahiri

2014

Journal of Biological Chemistry

163

101

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Background: BACE1 is the rate-limiting enzyme in the synthesis of A␤ from amyloid precursor protein.Results: Human miR-339-5p negatively regulates BACE1 and A␤ in human brain cultures and is reduced in AD specimens. Conclusion: Human miR-339-5p physiologically regulates human BACE1 protein expression and A␤ and is dysregulated in the AD brain. Significance: miR-339-5p represents a novel drug target in AD.

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MicroRNA-16 targets amyloid precursor protein to potentially modulate Alzheimer's-associated pathogenesis in SAMP8 mice

Cited by 164 publications

References 47 publications

Amyloid precursor protein regulates neurogenesis by antagonizing miR-574-5p in the developing cerebral cortex

Amyloid precursor protein regulates neurogenesis by antagonizing miR-574-5p in the developing cerebral cortex

MicroRNA-144 Is Regulated by Activator Protein-1 (AP-1) and Decreases Expression of Alzheimer Disease-related A Disintegrin and Metalloprotease 10 (ADAM10)

MicroRNA-339-5p Down-regulates Protein Expression of β-Site Amyloid Precursor Protein-Cleaving Enzyme 1 (BACE1) in Human Primary Brain Cultures and Is Reduced in Brain Tissue Specimens of Alzheimer Disease Subjects

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