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Stem Cells International
Volume 2017 (2017), Article ID 7617048, 10 pages
https://doi.org/10.1155/2017/7617048
Research Article

NURR1 Downregulation Favors Osteoblastic Differentiation of MSCs

1Department of Clinical and Experimental Medicine, Medical School, University of Foggia, Foggia, Italy
2Institute of Physical Chemistry, Department of Biophysical Chemistry, University of Heidelberg and Max Planck Institute for Intelligent Systems, Stuttgart, Germany
3Department of Basic and Medical Sciences, Neurosciences and Sense Organs, University of Bari, Bari, Italy
4IRCCS Istituto Tumori Giovannoi Paolo II, Bari, Italy
5Department of Emergency and Organ Transplantation, University of Bari, Bari, Italy

Correspondence should be addressed to Giorgio Mori; ti.gfinu@irom.oigroig

Received 30 April 2017; Accepted 12 June 2017; Published 9 July 2017

Academic Editor: Rajiv Saini

Copyright © 2017 Adriana Di Benedetto 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.

Abstract

Mesenchymal stem cells (MSCs) have been identified in human dental tissues. Dental pulp stem cells (DPSCs) were classified within MSC family, are multipotent, can be isolated from adult teeth, and have been shown to differentiate, under particular conditions, into various cell types including osteoblasts. In this work, we investigated how the differentiation process of DPSCs toward osteoblasts is controlled. Recent literature data attributed to the nuclear receptor related 1 (NURR1), a still unclarified role in osteoblast differentiation, while NURR1 is primarily involved in dopaminergic neuron differentiation and activity. Thus, in order to verify if NURR1 had a role in DPSC osteoblastic differentiation, we silenced it during all the processes and compared the expression of the main osteoblastic markers with control cultures. Our results showed that the inhibition of NURR1 significantly increased the expression of osteoblast markers collagen I and alkaline phosphatase. Further, in long time cultures, the mineral matrix deposition was strongly enhanced in NURR1-silenced cultures. These results suggest that NURR1 plays a key role in switching DPSC differentiation toward osteoblasts rather than neuronal or even other cell lines. In conclusion, DPSCs represent a source of osteoblast-like cells and downregulation of NURR1 strongly prompted their differentiation toward the osteoblastogenesis process.