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©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Transl Med. Dec 12, 2015; 4(3): 113-122
Published online Dec 12, 2015. doi: 10.5528/wjtm.v4.i3.113
Published online Dec 12, 2015. doi: 10.5528/wjtm.v4.i3.113
Pro- vs anti-stenotic capacities of type-I vs type-II human induced pluripotent-derived endothelial cells
Miwako Nishio, Masako Nakahara, Akira Yuo, Kumiko Saeki, Department of Disease Control, Research Institute, National Center for Global Health and Medicine, Tokyo 162-8655, Japan
Koichi Saeki, Section of Cell Engineering, Department of Basic Research, DNAVEC Center, ID Pharma Co., Ltd., Ibaraki 300-2611, Japan
Katsuhito Fujiu, Hiroshi Iwata, Ichiro Manabe, Department of Cardiovascular Medicine, Graduate School of Medicine, the University of Tokyo, Tokyo 113-8654, Japan
Katsuhito Fujiu, Translational Systems Biology and Medicine Initiative, the University of Tokyo, Tokyo 113-8654, Japan
Katsuhito Fujiu, Kumiko Saeki, PRESTO, Japan Science and Technology Agency, Saitama 332-0012, Japan
Author contributions: Nishio M and Nakahara M performed the experiments and analyzed the data; Saeki K contributed to the establishment of human iPS cells; Fujiu K, Iwata H, Manabe I and Yuo A coordinated the research; Saeki K designed the research and wrote the paper.
Supported by Grant-in-Aid from the Ministry of Health, Labour and Welfare of Japan (KHD1017); and by that from JST, PRESTO.
Institutional review board statement: All experiments including gene recombination experiments and animal experiments were performed after we had obtained permission from the review board of National Center for Global Health and Medicine.
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Institutional Animal Care and Use Committee of Research Institute, National Center for Global Health and Medicine, Tokyo, Japan (Authorization No. 15014).
Conflict-of-interest statement: None of the authors has any potential financial conflict of interest related to this manuscript.
Data sharing statement: Technical appendix and dataset are available from the corresponding author (saeki@ri.ncgm.go.jp).
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Kumiko Saeki, MD, PhD, Division Chief, Department of Disease Control, Research Institute, National Center for Global Health and Medicine, 1-21-1 Toyama Shinjukuiku, Tokyo 162-8655, Japan. saeki@ri.ncgm.go.jp
Telephone: +81-3-32027181 Fax: +81-3-32027364
Received: June 23, 2015
Peer-review started: June 29, 2015
First decision: August 25, 2015
Revised: October 16, 2015
Accepted: November 10, 2015
Article in press: November 11, 2015
Published online: December 12, 2015
Processing time: 175 Days and 0.4 Hours
Peer-review started: June 29, 2015
First decision: August 25, 2015
Revised: October 16, 2015
Accepted: November 10, 2015
Article in press: November 11, 2015
Published online: December 12, 2015
Processing time: 175 Days and 0.4 Hours
Core Tip
Core tip: We previously reported that human vascular endothelial cells (VECs) were classified into two categories by their in vitro effects on the proliferation of vascular smooth muscle cells: Pro-proliferative VECs (type-I) and anti-proliferative VECs (type-II). Applying our new technique to transplant human VECs onto the luminal surface of endothelial layer-removed murine arteries, the in vivo relevance of the concept for VEC categorization was validated. Transplantation of pro-proliferative VECs (type-I) resulted in total stenosis while that of anti-proliferative VECs (type-II) completely blocked the development of arteriostenosis. Thus, pro-stenosis (type-I) and anti-stenotic (type-II) capacities were verified in vivo.