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Treatment of Parkinson disease with C17.2 neural stem cells overexpressing NURR1 with a recombined republic‐deficit adenovirus containing the NURR1 gene
Author(s) -
Li QingJun,
Tang YaMei,
Liu Jun,
Zhou DaoYou,
Li XiangPen,
Xiao SongHua,
Jian DongXing,
Xing YiGang
Publication year - 2007
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.20449
Subject(s) - neural stem cell , biology , western blot , transfection , in situ hybridization , genetic enhancement , microbiology and biotechnology , stem cell , messenger rna , cancer research , gene , genetics
To study the potential benefit of the NURR1 gene in Parkinson's disease (PD), we constructed a recombinant republic‐deficit adenovirus containing the NURR1 gene (Ad‐NURR1) and expressed it in transplanted neural stem cells (NSC). Ad‐NURR1 was constructed, and NURR1 mRNA and protein expression were identified by in situ hybridization and western blot analysis, respectively. The identified NURR1 protein could directly or indirectly induce NSC differentiation into neurons. To identify a potential therapeutic use for the transfected NSCs, cells were transplanted into 6‐hydroxydopamine lesioned rats. Histopathological and behavioral alterations were evaluated via immunohistochemistry and the ration test, respectively, in rats transplanted with NSCs with or without the Ad‐NURR1 adenovirus. The Ad‐NURR1 construct effectively expressed the NURR1 protein, which could directly or indirectly induce NSC differentiation into neurons. Both histopathological and behavioral alterations were seen in rats treated with NSCs with or without the Ad‐NURR1 construct, although in the case of the latter, the benefits were more robust. These results suggest a potential therapeutic benefit for Ad‐NURR1‐expressing cells in the treatment of PD. The Ad‐NURR1 modification induced NSC differentiation and therefore represents a potential therapy for PD. Synapse 61:971–977, 2007. © 2007 Wiley‐Liss, Inc.