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.

scholarly journals Cyclic pulsation stress promotes bone formation of tissue engineered laminae through the F-actin/YAP-1/β-Catenin signaling axis

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Linli Li ◽  
Hailong Li ◽  
Yiqun He ◽  
Han Tang ◽  
Jian Dong ◽  
...  
Keyword(s):  
Bone Formation ◽  
Blood Vessel ◽  
Stromal Cells ◽  
Nuclear Translocation ◽  
Therapeutic Approaches ◽  
Blood Vessel Formation ◽  
Vessel Formation ◽  
Signaling Axis ◽  
Fluid Pulsation ◽  
Spinal Degeneration

AbstractMechanical loads are fundamental regulators of bone formation and remodeling. However, the molecular regulation of mechanotransduction during vertebral laminae regeneration remains poorly understood. Here, we found that cerebrospinal fluid pulsation (CSFP) stress—cyclic pulsation stress—could promote the osteogenic and angiogenic abilities of rat mesenchymal stromal cells (MSC), thereby promoting tissue-engineered laminae’s bone and blood vessel formation. In the process, F-actin relayed CSFP stress to promote the nuclear translocation of YAP1, which then decreased the degradation and promoted the nuclear translocation of β-Catenin. In turn, the nuclear translocation of β-Catenin promoted the osteogenic differentiation and angiogenic abilities of MSC, thereby promoting tissue-engineered laminae’s bone and blood vessel formation. Thus, we conclude that CSFP promotes the osteogenesis and angiogenesis of tissue-engineered laminae through the F-actin/YAP-1/β-Catenin signaling axis. This study advances our understanding of vertebral laminae regeneration and provides potential therapeutic approaches for spinal degeneration after spinal laminectomy.

scholarly journals ANGPTL3 Stimulates Endothelial Cell Adhesion and Migration via Integrin αvβ3 and Induces Blood Vessel Formation in Vivo

2002 ◽  
Vol 277 (19) ◽  
pp. 17281-17290 ◽  
Author(s):  
Gieri Camenisch ◽  
Maria Teresa Pisabarro ◽  
Daniel Sherman ◽  
Joe Kowalski ◽  
Mark Nagel ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Endothelial Cell ◽  
Blood Vessel ◽  
Integrin Αvβ3 ◽  
Blood Vessel Formation ◽  
Vessel Formation ◽  
Cell Adhesion And Migration ◽  
And Migration ◽  
Endothelial Cell Adhesion

Olfactomedin‐like 3 promotes PDGF‐dependent pericyte proliferation and migration during embryonic blood vessel formation

2020 ◽  
Vol 34 (11) ◽  
pp. 15559-15576
Author(s):  
Beat A. Imhof ◽  
Romain Ballet ◽  
Philippe Hammel ◽  
Stéphane Jemelin ◽  
Sarah Garrido‐Urbani ◽  
...  
Keyword(s):  
Blood Vessel ◽  
Blood Vessel Formation ◽  
Vessel Formation ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Bone marrow mononuclear cells are recruited to the sites of VEGF-induced neovascularization but are not incorporated into the newly formed vessels

Blood ◽  
2006 ◽  
Vol 107 (9) ◽  
pp. 3546-3554 ◽  
Author(s):  
Lorena Zentilin ◽  
Sabrina Tafuro ◽  
Serena Zacchigna ◽  
Nikola Arsic ◽  
Lucia Pattarini ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Blood Vessel ◽  
Mononuclear Cells ◽  
Ex Vivo ◽  
Experimental Models ◽  
Large Set ◽  
Blood Vessel Formation ◽  
Vessel Formation ◽  
Sprouting Angiogenesis ◽  
Vasculogenesis And Angiogenesis

Vascular endothelial growth factor (VEGF) is a key regulator of blood vessel formation during both vasculogenesis and angiogenesis. The prolonged expression of VEGF in the normoperfused skeletal muscles of adult rodents after gene transfer using AAV vectors induces the formation of a large set of new capillaries and small arteries. Notably, this process is accompanied by the massive infiltration by mononuclear cells. This observation raises the possibility that these cells might represent circulating progenitors that are eventually incorporated in the newly formed vessels. Here we explore this possibility by exploiting 4 different experimental models based on (a) the transplantation of male bone marrow into female recipients; (b) the transplantation of Tie2-GFP transgenic bone marrow; (c) the transplantation of bone marrow in the presence of erythropoietin (EPO), a mobilizer of endothelial progenitor cells (EPCs); and (d) the reimplantation of ex vivo–expanded EPCs. In all 4 models, VEGF acted as a powerful attractor of bone marrow–derived mononuclear cells, bearing different myeloid and endothelial markers proper of the EPCs to the sites of neovascularization. In no case, however, were the attracted cells incorporated in the newly formed vasculature. These observations indicate that new blood vessel formation induced by VEGF occurs through bona fide sprouting angiogenesis; the contribution of the infiltrating bone marrow–derived cells to this process still remains enigmatic.

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
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