Human models for smooth muscle cell differentiation. Focus on “A novel in vitro model system for smooth muscle differentiation from human embryonic stem cell-derived mesenchymal cells”

2013 ◽  
Vol 304 (4) ◽  
pp. C287-C288 ◽  
Author(s):  
Amy L. Firth ◽  
Jason X.-J. Yuan
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.


2007 ◽  
Vol 88 (11) ◽  
pp. 2977-2984 ◽  
Author(s):  
Don Stoltz ◽  
Renée Lapointe ◽  
Andrea Makkay ◽  
Michel Cusson

Unlike most viruses, the mature ichnovirus particle possesses two unit membrane envelopes. Following loss of the outer membrane in vivo, nucleocapsids are believed to gain entry into the cytosol via a membrane fusion event involving the inner membrane and the plasma membrane of susceptible host cells; accordingly, experimentally induced damage to the outer membrane might be expected to increase infectivity. Here, in an attempt to develop an in vitro model system for studying ichnovirus infection, we show that digitonin-induced disruption of the virion outer membrane not only increases infectivity, but also uncovers an activity not previously associated with any polydnavirus: fusion from without.


2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Iwan Jones ◽  
Tushar Devanand Yelhekar ◽  
Rebecca Wiberg ◽  
Paul J. Kingham ◽  
Staffan Johansson ◽  
...  

2011 ◽  
Vol 2 ◽  
Author(s):  
Michaela Keuper ◽  
Anna Dzyakanchuk ◽  
Kurt E. Amrein ◽  
Martin Wabitsch ◽  
Pamela Fischer-Posovszky

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