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Prospective Isolation of ISL1+ Cardiac Progenitors from Human ESCs for Myocardial Infarction Therapy

Title
Prospective Isolation of ISL1+ Cardiac Progenitors from Human ESCs for Myocardial Infarction Therapy
Authors
Ghazizadeh, Z.Fattahi, F.Mirzaei, M.Bayersaikhan, D.Lee, J.Chae, Se HyunHwang, Dae HeeByun, K.Tabar, M.S.Taleahmad, S.Mirshahvaladi, S.Shabani, P.Fonoudi, H.Haynes, P.A.Baharvand, H.Aghdami, N.Evans, T.Lee, B.Salekdeh, G.H.
DGIST Authors
Hwang, Dae Hee
Issue Date
2018-03
Citation
Stem Cell Reports, 10(3), 848-859
Type
Article
Article Type
Article
Keywords
cell therapymyocardial biologyproteomicsstem cells
ISSN
2213-6711
Abstract
The LIM-homeodomain transcription factor ISL1 marks multipotent cardiac progenitors that give rise to cardiac muscle, endothelium, and smooth muscle cells. ISL1+ progenitors can be derived from human pluripotent stem cells, but the inability to efficiently isolate pure populations has limited their characterization. Using a genetic selection strategy, we were able to highly enrich ISL1+ cells derived from human embryonic stem cells. Comparative quantitative proteomic analysis of enriched ISL1+ cells identified ALCAM (CD166) as a surface marker that enabled the isolation of ISL1+ progenitor cells. ALCAM+/ISL1+ progenitors are multipotent and differentiate into cardiomyocytes, endothelial cells, and smooth muscle cells. Transplantation of ALCAM+ progenitors enhances tissue recovery, restores cardiac function, and improves angiogenesis through activation of AKT-MAPK signaling in a rat model of myocardial infarction, based on cardiac MRI and histology. Our study establishes an efficient method for scalable purification of human ISL1+ cardiac precursor cells for therapeutic applications. In this article, Salekdeh and colleagues show that ISL1+ cardiac progenitors can be purified from a heterogeneous population of hESC-derived cardiomyocytes using ALCAM. Transplantation of multipotent ISL1+/ALCAM+ progenitors enhances tissue recovery, restores cardiac function, and improves angiogenesis in a rat model of myocardial infarction, based on cardiac MRI and histology. © 2018 The Authors
URI
http://hdl.handle.net/20.500.11750/6158
DOI
10.1016/j.stemcr.2018.01.037
Publisher
Cell Press
Files:
There are no files associated with this item.
Collection:
Department of New BiologySystems Biology and Medicine Lab1. Journal Articles


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