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Restoration of BDNF, DARPP32, and D2R Expression Following Intravenous Infusion of Human Immature Dental Pulp Stem Cells in Huntington’s Disease 3-NP Rat Model

Authors :
Cristiane Valverde Wenceslau
Dener Madeiro de Souza
Nicole Caroline Mambelli-Lisboa
Leandro Hideki Ynoue
Rodrigo Pinheiro Araldi
Joyce Macedo da Silva
Eduardo Pagani
Monica Santoro Haddad
Irina Kerkis
Source :
Cells, Vol 11, Iss 10, p 1664 (2022)
Publication Year :
2022
Publisher :
MDPI AG, 2022.

Abstract

Huntington’s disease (HD) is a neurodegenerative inherited genetic disorder, which leads to the onset of motor, neuropsychiatric and cognitive disturbances. HD is characterized by the loss of gamma-aminobutyric acid (GABA)ergic medium spiny neurons (MSNs). To date, there is no treatment for HD. Mesenchymal stem cells (MSCs) provide a substantial therapeutic opportunity for the HD treatment. Herein, we investigated the therapeutic potential of human immature dental pulp stem cells (hIDPSC), a special type of MSC originated from the neural crest, for HD treatment. Two different doses of hIDPSC were intravenously administrated in a subacute 3-nitropropionic acid (3NP)-induced rat model. We demonstrated hIDPSC homing in the striatum, cortex and subventricular zone using specific markers for human cells. Thirty days after hIDPSC administration, the cells found in the brain are still express hallmarks of undifferentiated MSC. Immunohistochemistry quantities analysis revealed a significant increase in the number of BDNF, DARPP32 and D2R positive stained cells in the striatum and cortex in the groups that received hIDPSC. The differences were more expressive in animals that received only one administration of hIDPSC. Altogether, these data suggest that the intravenous administration of hIDPSCs can restore the BDNF, DARPP32 and D2R expression, promoting neuroprotection and neurogenesis.

Details

Language :
English
ISSN :
20734409
Volume :
11
Issue :
10
Database :
Directory of Open Access Journals
Journal :
Cells
Publication Type :
Academic Journal
Accession number :
edsdoj.f53ee7f2e104c3ab6d9e5ebda8ae2ee
Document Type :
article
Full Text :
https://doi.org/10.3390/cells11101664