scholarly journals Human embryonic stem cell-derived mesenchymal cells preserve kidney function and extend lifespan in NZB/W F1 mouse model of lupus nephritis

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Austin Thiel ◽  
Gregory Yavanian ◽  
Maria-Dorothea Nastke ◽  
Peter Morales ◽  
Nicholas A. Kouris ◽  
...  
2011 ◽  
Vol 17 (11-12) ◽  
pp. 1537-1548 ◽  
Author(s):  
Nolan L. Boyd ◽  
Sara S. Nunes ◽  
Jenny D. Jokinen ◽  
Laxminarayanan Krishnan ◽  
Yinlu Chen ◽  
...  

2014 ◽  
Vol 20 (1-2) ◽  
pp. 365-377 ◽  
Author(s):  
Liisa T. Kuhn ◽  
Yongxing Liu ◽  
Nolan L. Boyd ◽  
James E. Dennis ◽  
Xi Jiang ◽  
...  

2011 ◽  
Vol 109 (1) ◽  
pp. 274-283 ◽  
Author(s):  
David L. Simpson ◽  
Nolan L. Boyd ◽  
Sunjay Kaushal ◽  
Steve L. Stice ◽  
Samuel C. Dudley

2013 ◽  
pp. 131015043635000 ◽  
Author(s):  
Sumati Sundaram ◽  
Andreana Echter ◽  
Amogh Sivarapatna ◽  
Caihong Qiu ◽  
Laura Niklason

2013 ◽  
Vol 304 (4) ◽  
pp. C289-C298 ◽  
Author(s):  
Xia Guo ◽  
Steven L. Stice ◽  
Nolan L. Boyd ◽  
Shi-You Chen

The objective of this study was to develop a novel in vitro model for smooth muscle cell (SMC) differentiation from human embryonic stem cell-derived mesenchymal cells (hES-MCs). We found that hES-MCs were differentiated to SMCs by transforming growth factor-β (TGF-β) in a dose- and time-dependent manner as demonstrated by the expression of SMC-specific genes smooth muscle α-actin, calponin, and smooth muscle myosin heavy chain. Under normal growth conditions, however, the differentiation capacity of hES-MCs was very limited. hES-MC-derived SMCs had an elongated and spindle-shaped morphology and contracted in response to the induction of carbachol and KCl. KCl-induced calcium transient was also evident in these cells. Compared with the parental cells, TGF-β-treated hES-MCs sustained the endothelial tube formation for a longer time due to the sustained SMC phenotype. Mechanistically, TGF-β-induced differentiation was both Smad- and serum response factor/myocardin dependent. TGF-β regulated myocardin expression via multiple signaling pathways including Smad2/3, p38 MAPK, and PI3K. Importantly, we found that a low level of myocardin was present in mesoderm prior to SMC lineage determination, and a high level of myocardin was not induced until the differentiation process was initiated. Taken together, our study characterized a novel SMC differentiation model that can be used for studying human SMC differentiation from mesoderm during vascular development.


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