Inhibition of new blood vessel formation in mice by systemic administration of human rib cartilage extract

1978 ◽  
Vol 34 (4) ◽  
pp. 490-491 ◽  
Author(s):  
M. Kamiński ◽  
Grażyna Kamińska ◽  
S. Majewski
Keyword(s):  
Blood Vessel ◽  
Systemic Administration ◽  
Blood Vessel Formation ◽  
Vessel Formation ◽  
Rib Cartilage

scholarly journals Emerging Role of AP-1 Transcription Factor JunB in Angiogenesis and Vascular Development

2021 ◽  
Vol 22 (6) ◽  
pp. 2804
Author(s):  
Yasuo Yoshitomi ◽  
Takayuki Ikeda ◽  
Hidehito Saito-Takatsuji ◽  
Hideto Yonekura
Keyword(s):  
Endothelial Cells ◽  
Transcription Factor ◽  
Blood Vessel ◽  
Vascular Endothelial Cells ◽  
Vascular Development ◽  
Endothelial Cell Migration ◽  
Vascular Endothelial ◽  
Blood Vessel Formation ◽  
Vessel Formation

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.

Blood vessel formation in the tissue-engineered bone with the constitutively active form of HIF-1α mediated BMSCs

Biomaterials ◽  
2012 ◽  
Vol 33 (7) ◽  
pp. 2097-2108 ◽  
Author(s):  
Duohong Zou ◽  
Zhiyuan Zhang ◽  
Jiacai He ◽  
Kai Zhang ◽  
Dongxia Ye ◽  
...  
Keyword(s):  
Blood Vessel ◽  
Active Form ◽  
Blood Vessel Formation ◽  
Vessel Formation ◽  
Constitutively Active

scholarly journals Trans-Resveratrol Inhibits Early Blood Vessel Formation (Vasculogenesis) Without Impairment of Embryonic Growth

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

scholarly journals Excess centrosomes perturb dynamic endothelial cell repolarization during blood vessel formation

2016 ◽  
Vol 27 (12) ◽  
pp. 1911-1920 ◽  
Author(s):  
Erich J. Kushner ◽  
Luke S. Ferro ◽  
Zhixian Yu ◽  
Victoria L. Bautch
Keyword(s):  
Blood Vessel ◽  
Stromal Cells ◽  
Cortical Microtubule ◽  
Interphase Cell ◽  
Blood Vessel Formation ◽  
Vessel Formation ◽  
Sprouting Angiogenesis ◽  
Actomyosin Contractility ◽  
Rac1 Activity ◽  
And Migration

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.

Mechanisms of Embryonic Blood Vessel Formation

1992 ◽  
pp. 353-354
Author(s):  
H. Drexler ◽  
H. Schurch ◽  
G. Breier ◽  
G. Drexler ◽  
W. Risau
Keyword(s):  
Blood Vessel ◽  
Blood Vessel Formation ◽  
Vessel Formation

Regulation of Embryonic Blood Vessel Formation

1992 ◽  
pp. 17-25
Author(s):  
Hannes Drexler ◽  
Harald Schnürch ◽  
Georg Breier ◽  
Werner Risau
Keyword(s):  
Blood Vessel ◽  
Blood Vessel Formation ◽  
Vessel Formation
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