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Title: Purification of functional human ES and iPSC-derived midbrain dopaminergic progenitors using LRTM1
Authors: Samata, Bumpei
Doi, Daisuke  kyouindb  KAKEN_id  orcid (unconfirmed)
Nishimura, Kaneyasu
Kikuchi, Tetsuhiro  kyouindb  KAKEN_id  orcid (unconfirmed)
Watanabe, Akira  kyouindb  KAKEN_id  orcid (unconfirmed)
Sakamoto, Yoshimasa
Kakuta, Jungo
Ono, Yuichi
Takahashi, Jun  kyouindb  KAKEN_id
Author's alias: 菊地, 哲広
髙橋, 淳
Issue Date: 14-Oct-2016
Publisher: Springer Nature
Journal title: Nature Communications
Volume: 7
Thesis number: 13097
Abstract: Human induced pluripotent stem cells (iPSCs) can provide a promising source of midbrain dopaminergic (mDA) neurons for cell replacement therapy for Parkinson's disease (PD). However, iPSC-derived donor cells inevitably contain tumorigenic or inappropriate cells. To eliminate these unwanted cells, cell sorting using antibodies for specific markers such as CORIN or ALCAM has been developed, but neither marker is specific for ventral midbrain. Here we employ a double selection strategy for cells expressing both CORIN and LMX1A::GFP, and report a cell surface marker to enrich mDA progenitors, LRTM1. When transplanted into 6-OHDA-lesioned rats, human iPSC-derived LRTM1 + cells survive and differentiate into mDA neurons in vivo, resulting in a significant improvement in motor behaviour without tumour formation. In addition, there was marked survival of mDA neurons following transplantation of LRTM1 + cells into the brain of an MPTP-treated monkey. Thus, LRTM1 may provide a tool for efficient and safe cell therapy for PD patients.
Rights: © 2016 The Author(s). This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit
DOI(Published Version): 10.1038/ncomms13097
PubMed ID: 27739432
Appears in Collections:Journal Articles

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