Hepatocyte growth factor plays a dual role in tendon‐derived stem cell proliferation, migration, and differentiation

2019 ◽  
Vol 234 (10) ◽  
pp. 17382-17391 ◽  
Author(s):  
Peilin Han ◽  
Qingbo Cui ◽  
Wenjun Lu ◽  
Shulong Yang ◽  
Manyu Shi ◽  
...  
Bone ◽  
2011 ◽  
Vol 49 (6) ◽  
pp. 1194-1204 ◽  
Author(s):  
Ketian Chen ◽  
Carlos Perez-Stable ◽  
Gianluca D'Ippolito ◽  
Paul C. Schiller ◽  
Bernard A. Roos ◽  
...  

2000 ◽  
Vol 275 (2) ◽  
pp. 1226-1232 ◽  
Author(s):  
Adolfo Garcia-Ocaña ◽  
Karen K. Takane ◽  
Mushtaq A. Syed ◽  
William M. Philbrick ◽  
Rupangi C. Vasavada ◽  
...  

Blood ◽  
2010 ◽  
Vol 115 (16) ◽  
pp. 3407-3412 ◽  
Author(s):  
Shai Y. Schubert ◽  
Alejandro Benarroch ◽  
Juan Monter-Solans ◽  
Elazer R. Edelman

Abstract Direct interaction of unactivated primary monocytes with endothelial cells induces a mitogenic effect in subconfluent, injured endothelial monolayers through activation of endothelial Met. We now report that monocytes' contact-dependent mitogenicity is controlled by activation-mediated regulation of hepatocyte growth factor. Direct interaction of unactivated monocytes with subconfluent endothelial cells for 12 hours resulted in 9- and 120-fold increase in monocyte tumor necrosis factor-α (TNFα) and interleukin-1β (IL-1β) mRNA levels and bitemporal spike in hepatocyte growth factor that closely correlates with endothelial Met and extracellular signal-related kinase (ERK) phosphorylation. Once activated, monocytes cannot induce a second wave of endothelial cell proliferation and endothelial Met phosphorylation and soluble hepatocyte growth factor levels fall off. Monocyte-induced proliferation is dose dependent and limited to the induction of a single cell cycle. Monocytes retain their ability to activate other endothelial cells for up to 8 hours after initial interaction, after which they are committed to the specific cell. There is therefore a profoundly sophisticated mode of vascular repair. Confluent endothelial cells ensure vascular quiescence, whereas subconfluence promotes vessel activation. Simultaneously, circulating monocytes stimulate endothelial cell proliferation, but lose this potential once activated. Such a system provides for the fine balance that can restore vascular and endothelial homeostasis with minimal overcompensation.


Stem Cells ◽  
2009 ◽  
Vol 27 (2) ◽  
pp. 408-419 ◽  
Author(s):  
Camille Nicoleau ◽  
Omar Benzakour ◽  
Fabienne Agasse ◽  
Nathalie Thiriet ◽  
Jérôme Petit ◽  
...  

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