http://www.cnr.it/ontology/cnr/individuo/prodotto/ID5023

MicroRNA-101 regulates amyloid precursor protein expression in hippocampal neurons (Articolo in rivista)

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MicroRNA-101 regulates amyloid precursor protein expression in hippocampal neurons (Articolo in rivista) (literal)

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Alternative label

Vilardo E.1), Barbato C.1), 2), Ciotti M.T.1), Cogoni C.2), 3), Ruberti F.1) (2010)
MicroRNA-101 regulates amyloid precursor protein expression in hippocampal neurons
in Journal of biological chemistry (Online); American society for biochemistry and molecular biology, Baltimore (Stati Uniti d'America)
(literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

Vilardo E.1), Barbato C.1), 2), Ciotti M.T.1), Cogoni C.2), 3), Ruberti F.1) (literal)

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Note

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1) - INMM-Istituto di Neurobiologia e Medicina Molecolare, CNR, Via del Fosso di Fiorano, 64/65, 00143 Roma, Italy; 2) - EBRI-European Brain Research Institute-Fondazione EBRI-Rita Levi-Montalcini, Via del Fosso di Fiorano, 64/65, 00143 Roma, Italy; 3) - Dipartimento di Biotecnologie Cellulari ed Ematologia, Università di Roma La Sapienza, Viale Regina Elena, 324, 00161 Roma, Italy. (literal)

Titolo

MicroRNA-101 regulates amyloid precursor protein expression in hippocampal neurons (literal)

Abstract

The amyloid precursor protein (APP) and its proteolytic product amyloid beta (A²) are associated with both familial and sporadic forms of Alzheimer disease (AD). Aberrant expression and function of microRNAs has been observed in AD. Here, we show that in rat hippocampal neurons cultured in vitro, the down-regulation of Argonaute-2, a key component of the RNA-induced silencing complex, produced an increase in APP levels. Using site-directed mutagenesis, a microRNA responsive element (RE) for miR-101 was identified in the 32-untranslated region (UTR) of APP. The inhibition of endogenous miR-101 increased APP levels, whereas lentiviral-mediated miR-101 overexpression significantly reduced APP and A² load in hippocampal neurons. In addition, miR-101 contributed to the regulation of APP in response to the proinflammatory cytokine interleukin-1² (IL-l²). Thus, miR-101 is a negative regulator of APP expression and affects the accumulation of A², suggesting a possible role for miR-101 in neuropathological conditions. (literal)

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