NPY modulates miR-30a-5p and BDNF in opposite direction in an in vitro model of Alzheimer disease: A possible role in neuroprotection?

Nicoletta Croce, Francesca Gelfo, Maria Teresa Ciotti, Giorgio Federici, Carlo Caltagirone, Sergio Bernardini, Francesco Angelucci

Research output: Contribution to journalArticle

Abstract

Using in vitro models of Alzheimer's disease (AD), we found that the toxic effects of amyloid beta 25-35 (Aβ25-35) on the neurotrophin brain-derived neurotrophic factor (BDNF) were counteracted by pre-incubation with neuropeptide Y (NPY), a neuropeptide expressed within the central nervous system. Nonetheless, the mechanism of action of NPY on BDNF neuronal production in the presence of Aβ is not known. BDNF expression might be directly regulated by microRNA (miRs), small non-coding DNA fragments that regulate the expression of target genes. Thus, there is the possibility that miRs alterations are present in AD-affected neurons and that NPY influences miR expression. To test this hypothesis, we exposed NPY-pretreated primary rat cortical neurons to Aβ25-35 and measured miR-30a-5p (a member of the miR-30a family involved in BDNF tuning expression) and BDNF mRNA and protein expression after 24 and 48 h. Our results demonstrated that pre-treatment with NPY decreased miR-30a-5p expression and increased BDNF mRNA and protein expression at 24 and 48 h of incubation with Aβ. Therefore, this study demonstrates that NPY modulates BDNF and its regulating microRNA miR-30a-5p in opposite direction with a mechanism that possibly contributes to the neuroprotective effect of NPY in rat cortical neurons exposed to Aβ.

Original languageEnglish
Pages (from-to)189-195
Number of pages7
JournalMolecular and Cellular Biochemistry
Volume376
Issue number1-2
DOIs
Publication statusPublished - Apr 2013

Keywords

  • Alzheimer disease
  • BDNF
  • miR-30a-5p
  • NPY
  • Primary cortical neurons

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Molecular Biology
  • Cell Biology

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