scholarly journals Canonical Wnt Signaling Promotes Neovascularization Through Determination of Endothelial Progenitor Cell Fate via Metabolic Profile Regulation

Stem Cells ◽  
2019 ◽  
Vol 37 (10) ◽  
pp. 1331-1343 ◽  
Author(s):  
Yan Shao ◽  
Jianglei Chen ◽  
Willard Freeman ◽  
Li-Jie Dong ◽  
Zhi-Hui Zhang ◽  
...  
2019 ◽  
Vol 46 (1) ◽  
pp. 14-25 ◽  
Author(s):  
V. V. Kozin ◽  
I. E. Borisenko ◽  
R. P. Kostyuchenko

2014 ◽  
Vol 207 (5) ◽  
pp. 657-671 ◽  
Author(s):  
Pallavi Bhattaram ◽  
Alfredo Penzo-Méndez ◽  
Kenji Kato ◽  
Kaustav Bandyopadhyay ◽  
Abhilash Gadi ◽  
...  

Canonical WNT signaling stabilizes β-catenin to determine cell fate in many processes from development onwards. One of its main roles in skeletogenesis is to antagonize the chondrogenic transcription factor SOX9. We here identify the SOXC proteins as potent amplifiers of this pathway. The SOXC genes, i.e., Sox4, Sox11, and Sox12, are coexpressed in skeletogenic mesenchyme, including presumptive joints and perichondrium, but not in cartilage. Their inactivation in mouse embryo limb bud caused massive cartilage fusions, as joint and perichondrium cells underwent chondrogenesis. SOXC proteins govern these cells cell autonomously. They replace SOX9 in the adenomatous polyposis coli–Axin destruction complex and therein inhibit phosphorylation of β-catenin by GSK3. This inhibition, a crucial, limiting step in canonical WNT signaling, thus becomes a constitutive event. The resulting SOXC/canonical WNT-mediated synergistic stabilization of β-catenin contributes to efficient repression of Sox9 in presumptive joint and perichondrium cells and thereby ensures proper delineation and articulation of skeletal primordia. This synergy may determine cell fate in many processes besides skeletogenesis.


Author(s):  
Brian A. Kinney ◽  
Richard H. Row ◽  
Yu-Jung Tseng ◽  
Maxwell D. Weidmann ◽  
Holger Knaut ◽  
...  

AbstractAnimal embryogenesis requires a precise coordination between morphogenesis and cell fate specification. It is unclear if there are mechanisms that prevent uncoupling of these processes to ensure robust development. During mesoderm induction, mesodermal fate acquisition is tightly coordinated with the morphogenetic process of epithelial to mesenchymal transition (EMT). In zebrafish, cells exist transiently in a partial EMT state during mesoderm induction. Here we show that cells expressing the neural inducing transcription factor Sox2 are held in the partial EMT state, stopping them from completing the EMT and joining the mesodermal territory. This is critical for preventing ectopic neural tissue from forming. The mechanism involves specific interactions between Sox2 and the mesoderm inducing canonical Wnt signaling pathway. When Wnt signaling is inhibited in Sox2 expressing cells trapped in the partial EMT, cells are now able to exit into the mesodermal territory, but form an ectopic spinal cord instead of mesoderm. Our work identifies a critical developmental checkpoint that ensures that morphogenetic movements establishing the mesodermal germ layer are accompanied by robust mesodermal cell fate acquisition.


2013 ◽  
Vol 54 (12) ◽  
pp. 7386 ◽  
Author(s):  
Xiaochen Liu ◽  
Jeffrey McBride ◽  
Yueping Zhou ◽  
Zuguo Liu ◽  
Jian-xing Ma

PLoS ONE ◽  
2009 ◽  
Vol 4 (4) ◽  
pp. e5388 ◽  
Author(s):  
Emily J. Arnsdorf ◽  
Padmaja Tummala ◽  
Christopher R. Jacobs

2007 ◽  
Vol 308 (2) ◽  
pp. 392-406 ◽  
Author(s):  
Rhonda N.T. Lassiter ◽  
Carolynn M. Dude ◽  
Stephanie B. Reynolds ◽  
Nichelle I. Winters ◽  
Clare V.H. Baker ◽  
...  

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