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MicroRNA-101 regulates amyloid precursor protein expression in hippocampal neurons

Elisa Vilardo1, Christian Barbato, Mariateresa Ciotti

  • 1Istituto di Neurobiologia e Medicina Molecolare, CNR, Roma, Italy.

The Journal of Biological Chemistry
|April 17, 2010
PubMed

Insights

MicroRNA-101 (miR-101) regulates amyloid precursor protein (APP) levels, impacting amyloid beta (Abeta) accumulation in Alzheimer disease (AD) models. This microRNA offers a potential therapeutic target for AD neuropathology.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Alzheimer disease (AD) is linked to amyloid precursor protein (APP) and amyloid beta (Abeta).
  • Dysregulated microRNA (miRNA) expression is implicated in AD pathogenesis.
  • Argonaute-2, a key RNA-induced silencing complex protein, influences APP levels.

Purpose of the Study:

  • To investigate the role of microRNA-101 (miR-101) in regulating APP expression.
  • To determine miR-101's effect on amyloid beta (Abeta) accumulation in neurons.
  • To explore miR-101's involvement in the response to interleukin-1beta (IL-1beta).

Main Methods:

  • Site-directed mutagenesis to identify miR-101 responsive elements in the APP 3'-untranslated region (UTR).
  • In vitro culture of rat hippocampal neurons.
  • Manipulation of miR-101 levels using inhibition and lentiviral overexpression; assessment of APP and Abeta levels.

Main Results:

  • Down-regulation of Argonaute-2 increased APP levels.
  • Inhibition of endogenous miR-101 led to elevated APP levels.
  • miR-101 overexpression significantly reduced APP and Abeta load in hippocampal neurons.
  • miR-101 mediated APP regulation in response to IL-1beta.

Conclusions:

  • miR-101 acts as a negative regulator of APP expression.
  • miR-101 influences the accumulation of Abeta, a key factor in Alzheimer disease.
  • miR-101 presents a potential therapeutic target for neuropathological conditions like AD.

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