MicroRNAs targeting Nicastrin regulate Aβ production and are affected by target site polymorphisms
Identifieur interne : 000078 ( France/Analysis ); précédent : 000077; suivant : 000079MicroRNAs targeting Nicastrin regulate Aβ production and are affected by target site polymorphisms
Auteurs : Charlotte Delay [Canada, France] ; Véronique Dorval [Canada] ; Alice Fok [Canada] ; Benjamin Grenier-Boley [France] ; Jean-Charles Lambert [France] ; G.-Y. Hsiung [Canada] ; Sébastien S. Hébert [Canada]Source :
- Frontiers in Molecular Neuroscience [ 1662-5099 ] ; 2014.
Abstract
Despite the growing number of genome-wide association studies, the involvement of polymorphisms in microRNA target sites (polymiRTS) in Alzheimer’s disease (AD) remains poorly investigated. Recently, we have shown that AD-associated single-nucleotide polymorphisms (SNPs) present in the 3′ untranslated region (3′UTR) of amyloid precursor protein (APP) could directly affect miRNA function. In theory, loss of microRNA (miRNA) function could lead to risk for AD by increasing APP expression and Aβ peptide production. In this study, we tested the hypothesis that Nicastrin, a γ-secretase subunit involved in Aβ generation, could be regulated by miRNAs, and consequently affected by 3′UTR polymorphisms. Bioinformatic analysis identified 22 putative miRNA binding sites located in or near Nicastrin 3′UTR polymorphisms. From these miRNA candidates, six were previously shown to be expressed in human brain. We identified miR-24, miR-186, and miR-455 as regulators of Nicastrin expression, both
Url:
DOI: 10.3389/fnmol.2014.00067
PubMed: 25100943
PubMed Central: 4103510
Affiliations:
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PMC:4103510Le document en format XML
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uniqKey="Dorval V" first="Véronique" last="Dorval">Véronique Dorval</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Axe Neurosciences, Centre de Recherche du CHU de Québec, Université Laval, Québec</institution><country>QC, Canada</country></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea></wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Département de Psychiatrie et de Neurosciences, Faculté de Médecine, Université Laval, Québec</institution><country>QC, Canada</country></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea></wicri:regionArea></affiliation></author><author><name sortKey="Fok, Alice" sort="Fok, Alice" uniqKey="Fok A" first="Alice" last="Fok">Alice Fok</name><affiliation wicri:level="1"><nlm:aff id="aff4"><institution>Division of Neurology, Department of Medicine, University of British Columbia</institution><country>Vancouver, QC, Canada</country></nlm:aff><country 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xml:lang="fr">France</country><wicri:regionArea></wicri:regionArea></affiliation></author><author><name sortKey="Hsiung, G Y" sort="Hsiung, G Y" uniqKey="Hsiung G" first="G.-Y." last="Hsiung">G.-Y. Hsiung</name><affiliation wicri:level="1"><nlm:aff id="aff4"><institution>Division of Neurology, Department of Medicine, University of British Columbia</institution><country>Vancouver, QC, Canada</country></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea></wicri:regionArea></affiliation></author><author><name sortKey="Hebert, Sebastien S" sort="Hebert, Sebastien S" uniqKey="Hebert S" first="Sébastien S." last="Hébert">Sébastien S. Hébert</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Axe Neurosciences, Centre de Recherche du CHU de Québec, Université Laval, Québec</institution><country>QC, Canada</country></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea></wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Département de Psychiatrie et de Neurosciences, Faculté de Médecine, Université Laval, Québec</institution><country>QC, Canada</country></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea></wicri:regionArea></affiliation></author></analytic><series><title level="j">Frontiers in Molecular Neuroscience</title><idno type="eISSN">1662-5099</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Despite the growing number of genome-wide association studies, the involvement of polymorphisms in microRNA target sites (polymiRTS) in Alzheimer’s disease (AD) remains poorly investigated. Recently, we have shown that AD-associated single-nucleotide polymorphisms (SNPs) present in the 3′ untranslated region (3′UTR) of amyloid precursor protein (APP) could directly affect miRNA function. In theory, loss of microRNA (miRNA) function could lead to risk for AD by increasing APP expression and Aβ peptide production. In this study, we tested the hypothesis that Nicastrin, a γ-secretase subunit involved in Aβ generation, could be regulated by miRNAs, and consequently affected by 3′UTR polymorphisms. Bioinformatic analysis identified 22 putative miRNA binding sites located in or near Nicastrin 3′UTR polymorphisms. From these miRNA candidates, six were previously shown to be expressed in human brain. We identified miR-24, miR-186, and miR-455 as regulators of Nicastrin expression, both <italic>in vitro</italic> and under physiological conditions in human cells, which resulted in altered Aβ secretion. Using luciferase-based assays, we further demonstrated that rs113810300 and rs141849450 SNPs affected miRNA-mediated repression of Nicastrin. Notably, rs141849450 completely abolished the miR-455-mediated repression of Nicastrin. Finally, the rs141849450 variant was identified in 1 out of 511 AD cases but not in 631 controls. These observations set the stage for future studies exploring the role of miRNAs and 3′UTR polymorphisms in AD.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Ambros, V" uniqKey="Ambros V">V. Ambros</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Betel, D" uniqKey="Betel D">D. Betel</name></author><author><name sortKey="Wilson, M" uniqKey="Wilson M">M. Wilson</name></author><author><name sortKey="Gabow, A" uniqKey="Gabow A">A. Gabow</name></author><author><name sortKey="Marks, D S" uniqKey="Marks D">D. S. 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Zhang</name></author><author><name sortKey="Fortin, Y" uniqKey="Fortin Y">Y. Fortin</name></author><author><name sortKey="Wang, E" uniqKey="Wang E">E. Wang</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Canada</li><li>France</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Delay, Charlotte" sort="Delay, Charlotte" uniqKey="Delay C" first="Charlotte" last="Delay">Charlotte Delay</name></noRegion><name sortKey="Delay, Charlotte" sort="Delay, Charlotte" uniqKey="Delay C" first="Charlotte" last="Delay">Charlotte Delay</name><name sortKey="Dorval, Veronique" sort="Dorval, Veronique" uniqKey="Dorval V" first="Véronique" last="Dorval">Véronique Dorval</name><name sortKey="Dorval, Veronique" sort="Dorval, Veronique" uniqKey="Dorval V" first="Véronique" last="Dorval">Véronique Dorval</name><name sortKey="Fok, Alice" sort="Fok, Alice" uniqKey="Fok A" first="Alice" last="Fok">Alice Fok</name><name sortKey="Hebert, Sebastien S" sort="Hebert, Sebastien S" uniqKey="Hebert S" first="Sébastien S." last="Hébert">Sébastien S. Hébert</name><name sortKey="Hebert, Sebastien S" sort="Hebert, Sebastien S" uniqKey="Hebert S" first="Sébastien S." last="Hébert">Sébastien S. Hébert</name><name sortKey="Hsiung, G Y" sort="Hsiung, G Y" uniqKey="Hsiung G" first="G.-Y." last="Hsiung">G.-Y. Hsiung</name></country><country name="France"><noRegion><name sortKey="Delay, Charlotte" sort="Delay, Charlotte" uniqKey="Delay C" first="Charlotte" last="Delay">Charlotte Delay</name></noRegion><name sortKey="Grenier Boley, Benjamin" sort="Grenier Boley, Benjamin" uniqKey="Grenier Boley B" first="Benjamin" last="Grenier-Boley">Benjamin Grenier-Boley</name><name sortKey="Lambert, Jean Charles" sort="Lambert, Jean Charles" uniqKey="Lambert J" first="Jean-Charles" last="Lambert">Jean-Charles Lambert</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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