HOXC9: A Key Regulator of Endothelial Cell Quiescence and Vascular Morphogenesis

2012 ◽  
Vol 22 (1) ◽  
pp. 7-11 ◽  
Author(s):  
Sandra Jasmin Stoll ◽  
Jens Kroll
Blood ◽  
2011 ◽  
Vol 118 (15) ◽  
pp. 4274-4284 ◽  
Author(s):  
Feng Zhang ◽  
Jarett E. Michaelson ◽  
Simon Moshiach ◽  
Norman Sachs ◽  
Wenyuan Zhao ◽  
...  

Abstract Tetraspanin CD151 is highly expressed in endothelial cells and regulates pathologic angiogenesis. However, the mechanism by which CD151 promotes vascular morphogenesis and whether CD151 engages other vascular functions are unclear. Here we report that CD151 is required for maintaining endothelial capillary-like structures formed in vitro and the integrity of endothelial cell-cell and cell-matrix contacts in vivo. In addition, vascular permeability is markedly enhanced in the absence of CD151. As a global regulator of endothelial cell-cell and cell-matrix adhesions, CD151 is needed for the optimal functions of various cell adhesion proteins. The loss of CD151 elevates actin cytoskeletal traction by up-regulating RhoA signaling and diminishes actin cortical meshwork by down-regulating Rac1 activity. The inhibition of RhoA or activation of cAMP signaling stabilizes CD151-silenced or -null endothelial structure in vascular morphogenesis. Together, our data demonstrate that CD151 maintains vascular stability by promoting endothelial cell adhesions, especially cell-cell adhesion, and confining cytoskeletal tension.


2015 ◽  
Vol 35 (12) ◽  
pp. 2626-2637 ◽  
Author(s):  
Bahman Rostama ◽  
Jacqueline E. Turner ◽  
Guy T. Seavey ◽  
Christine R. Norton ◽  
Thomas Gridley ◽  
...  

2012 ◽  
Vol 303 (7) ◽  
pp. C743-C756 ◽  
Author(s):  
Sejeong Shin ◽  
Laura Wolgamott ◽  
Sang-Oh Yoon

Vascular morphogenesis is a key process for development, reproduction, and pathogenesis. Thus understanding the mechanisms of this process is of pathophysiological importance. Despite the fact that collagen I is the most abundant and potent promorphogenic molecule known, the molecular mechanisms by which this protein regulates endothelial cell tube morphogenesis are still unclear. Here we provide strong evidence that collagen I induces tube morphogenesis by inhibiting glycogen synthase kinase 3β (GSK3β). Further mechanistic studies revealed that GSK3β activity is regulated by protein kinase D (PKD). PKD inhibited GSK3β activity, which was required for collagen I-induced endothelial tube morphogenesis. We also found that GSK3β regulated trafficking of integrin α2β1 in a Rab11-dependent manner. Taken together, our studies highlight the important role of PKD in the regulation of collagen I-induced vascular morphogenesis and show that it is mediated by the modulation of GSK3β activity and integrin α2β1 trafficking.


2020 ◽  
Vol 2 (1) ◽  
pp. H29-H43
Author(s):  
Catarina G Fonseca ◽  
Pedro Barbacena ◽  
Claudio A Franco

The vascular system is a hierarchically organized network of blood vessels that play crucial roles in embryogenesis, homeostasis and disease. Blood vessels are built by endothelial cells – the cells lining the interior of blood vessels – through a process named vascular morphogenesis. Endothelial cells react to different biomechanical signals in their environment by adjusting their behavior to: (1) invade, proliferate and fuse to form new vessels (angiogenesis); (2) remodel, regress and establish a hierarchy in the network (patterning); and (3) maintain network stability (quiescence). Each step involves the coordination of endothelial cell differentiation, proliferation, polarity, migration, rearrangements and shape changes to ensure network integrity and an efficient barrier between blood and tissues. In this review, we highlighted the relevance and the mechanisms involving endothelial cell migration during different steps of vascular morphogenesis. We further present evidence on how impaired endothelial cell dynamics can contribute to pathology.


2014 ◽  
Vol 5 (1) ◽  
pp. 23 ◽  
Author(s):  
Torbjorn O Pedersen ◽  
Anna L Blois ◽  
Ying Xue ◽  
Zhe Xing ◽  
Yang Sun ◽  
...  

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