Coronary stents with inducible VEGF/HGFsecreting UCB-MSCs reduced restenosis and increased re-endothelialization in a swine model

Title
Coronary stents with inducible VEGF/HGFsecreting UCB-MSCs reduced restenosis and increased re-endothelialization in a swine model
Authors
정윤기정미진장현경김평환김동욱조현민김대환임경섭김한별임한철한동근홍영준조제열
Issue Date
2018-09
Publisher
Experimental & molecular medicine
Citation
VOL 50-114-14
Abstract
Atherosclerotic plaques within the vasculature may eventually lead to heart failure. Currently, cardiac stenting is the most effective and least invasive approach to treat this disease. However, in-stent restenosis is a complex chronic side effect of stenting treatment. This study used coronary stents coated with stem cells secreting angiogenic growth factors via an inducible genome-editing system to reduce stent restenosis and induce re-endothelialization within the artery. The characteristics of the cells and their adhesion properties on the stents were confirmed, and the stents were transplanted into a swine model to evaluate restenosis and the potential therapeutic use of stents with stem cells. Restenosis was evaluated using optical coherence tomography (OCT), microcomputed tomography (mCT) and angiography, and re-endothelialization was evaluated by immunostaining after cardiac stent treatment. Compared to a bare metal stent (BMS) or a parental umbilical cord blood-derived mesenchymal stem cell (UCB-MSC)-coated stent, the stents with stem cells capable of the controlled release of hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) successfully reduced restenosis within the stent and induced natural re-endothelialization. Furthermore, UCB-MSCs exhibited the ability to differentiate into endothelial cells in Matrigel, and HGF and VEGF improved this differentiation. Our study indicates that stents coated with UCB-MSCs secreting VEGF/HGF reduce the restenosis side effects of cardiac stenting with improved re-endothelialization.
URI
http://pubs.kist.re.kr/handle/201004/68974
ISSN
1226-3613
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KIST Publication > Article
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