Abstract P009: Correlation between immune modulation of macrophage recruitment and new blood vessel formation in a subcutaneous murine mouse model of colorectal cancer

Author(s):  
Shelby N. Bess ◽  
Timothy J. Muldoon
Molecules ◽  
2014 ◽  
Vol 19 (11) ◽  
pp. 17578-17603 ◽  
Author(s):  
Mozhgan Kanavi ◽  
Soesiawati Darjatmoko ◽  
Shoujian Wang ◽  
Amir Azari ◽  
Mitra Farnoodian ◽  
...  

2010 ◽  
Vol 27 (5) ◽  
pp. 767-774 ◽  
Author(s):  
Jangwook Lee ◽  
Suk Ho Bhang ◽  
Honghyun Park ◽  
Byung-Soo Kim ◽  
Kuen Yong Lee

2021 ◽  
Vol 22 (6) ◽  
pp. 2804
Author(s):  
Yasuo Yoshitomi ◽  
Takayuki Ikeda ◽  
Hidehito Saito-Takatsuji ◽  
Hideto Yonekura

Blood vessels are essential for the formation and maintenance of almost all functional tissues. They play fundamental roles in the supply of oxygen and nutrition, as well as development and morphogenesis. Vascular endothelial cells are the main factor in blood vessel formation. Recently, research findings showed heterogeneity in vascular endothelial cells in different tissue/organs. Endothelial cells alter their gene expressions depending on their cell fate or angiogenic states of vascular development in normal and pathological processes. Studies on gene regulation in endothelial cells demonstrated that the activator protein 1 (AP-1) transcription factors are implicated in angiogenesis and vascular development. In particular, it has been revealed that JunB (a member of the AP-1 transcription factor family) is transiently induced in endothelial cells at the angiogenic frontier and controls them on tip cells specification during vascular development. Moreover, JunB plays a role in tissue-specific vascular maturation processes during neurovascular interaction in mouse embryonic skin and retina vasculatures. Thus, JunB appears to be a new angiogenic factor that induces endothelial cell migration and sprouting particularly in neurovascular interaction during vascular development. In this review, we discuss the recently identified role of JunB in endothelial cells and blood vessel formation.


Biomaterials ◽  
2012 ◽  
Vol 33 (7) ◽  
pp. 2097-2108 ◽  
Author(s):  
Duohong Zou ◽  
Zhiyuan Zhang ◽  
Jiacai He ◽  
Kai Zhang ◽  
Dongxia Ye ◽  
...  

2008 ◽  
Vol 107 (2) ◽  
pp. 118-127 ◽  
Author(s):  
Paulo Fernando Dias ◽  
Fernanda Vieira Berti ◽  
Jarbas Mota Siqueira Jr ◽  
Marcelo Maraschin ◽  
Antônio Ricardo Gagliardi ◽  
...  

2016 ◽  
Vol 27 (12) ◽  
pp. 1911-1920 ◽  
Author(s):  
Erich J. Kushner ◽  
Luke S. Ferro ◽  
Zhixian Yu ◽  
Victoria L. Bautch

Blood vessel formation requires dynamic movements of endothelial cells (ECs) within sprouts. The cytoskeleton regulates migratory polarity, and centrosomes organize the microtubule cytoskeleton. However, it is not well understood how excess centrosomes, commonly found in tumor stromal cells, affect microtubule dynamics and interphase cell polarity. Here we find that ECs dynamically repolarize during sprouting angiogenesis, and excess centrosomes block repolarization and reduce migration and sprouting. ECs with excess centrosomes initially had more centrosome-derived microtubules but, paradoxically, fewer steady-state microtubules. ECs with excess centrosomes had elevated Rac1 activity, and repolarization was rescued by blockade of Rac1 or actomyosin blockers, consistent with Rac1 activity promoting cortical retrograde actin flow and actomyosin contractility, which precludes cortical microtubule engagement necessary for dynamic repolarization. Thus normal centrosome numbers are required for dynamic repolarization and migration of sprouting ECs that contribute to blood vessel formation.


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