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Stem Cells International
Volume 2017, Article ID 5274171, 11 pages
Research Article

β-Arrestin1/miR-326 Transcription Unit Is Epigenetically Regulated in Neural Stem Cells Where It Controls Stemness and Growth Arrest

1Department of Molecular Medicine, Sapienza University of Rome, Rome, Italy
2Department of Experimental Medicine, Sapienza University of Rome, Rome, Italy
3Department of Radiological, Oncological and Anatomopathological Sciences, Sapienza University of Rome, Rome, Italy
4IRCCS Neuromed, Pozzilli, Italy
5Department of Hematology/Oncology and Stem Cell Transplantation, Bambino Gesù Children’s Hospital, IRCCS, Rome, Italy
6Center for Life NanoScience@Sapienza, Istituto Italiano di Tecnologia, Rome, Italy

Correspondence should be addressed to Elisabetta Ferretti; ti.1amorinu@itterref.attebasile

Received 4 November 2016; Revised 2 January 2017; Accepted 15 January 2017; Published 12 February 2017

Academic Editor: Jinsong Zhang

Copyright © 2017 Agnese Po et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Cell development is regulated by a complex network of mRNA-encoded proteins and microRNAs, all funnelling onto the modulation of self-renewal or differentiation genes. How intragenic microRNAs and their host genes are transcriptionally coregulated and their functional relationships for the control of neural stem cells (NSCs) are poorly understood. We propose here the intragenic miR-326 and its host gene β-arrestin1 as novel players whose epigenetic silencing maintains stemness in normal cerebellar stem cells. Such a regulation is mediated by CpG islands methylation of the common promoter. Epigenetic derepression of β-arrestin1/miR-326 by differentiation signals or demethylating agents leads to suppression of stemness features and cell growth and promotes cell differentiation. β-Arrestin1 inhibits cell proliferation by enhancing the nuclear expression of the cyclin-dependent kinase inhibitor p27. Therefore, we propose a new mechanism for the control of cerebellar NSCs where a coordinated epigenetic mechanism finely regulates β-arrestin1/miR-326 expression and consequently NSCs stemness and cell growth.