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.

Abstract 182: Inhibitor of differentiation (Id)3 Regulation of the Vasculature in Adipose Tissue

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Victoria Osinski ◽  
Jennifer Kirby ◽  
Swapnil Sonkusare ◽  
Mete Civelek ◽  
Coleen McNamara
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Adipose Tissue ◽  
Blood Vessel ◽  
Vascular Development ◽  
Tissue Expansion ◽  
Dependent Manner ◽  
Blood Vessel Formation ◽  
Vessel Formation ◽  
Helix Loop Helix

Rationale: Over half of the U.S. is overweight or obese and excessive weight gain greatly increases one’s risk of cardiovascular disease. Adipose tissue requires new blood vessel formation to support transport of nutrients during expansion. Our lab has previously published that global loss of the helix-loop-helix transcription factor Inhibitor of differentiation 3 (Id3) results in attenuated increases in adipose depot size and microvascular blood volume in mice fed a high fat diet (HFD). Id3 has also been implicated in regulating tumor angiogenesis. Together, our results suggest that Id3 is regulating HFD-induced angiogenesis in adipose tissue. Methods and Results: To determine if Id3 is regulating angiogenesis, we performed genetic, cellular, and arterial experiments and analyses. Using bromodeoxyuridine (BrdU) treatments and flow cytometry, we found that endothelial cells within adipose tissue of mice with a global genetic knockout of Id3 (Id3 KO) had fewer proliferating (BrdU-positive) endothelial cells (0.0679% BrdU+CD31+ cells) than wild type (WT) mice (0.754% BrdU+CD31+). Using mouse adipose tissue gene expression data from the Gene Ontology Consortium database, we found that genes correlating most significantly with Id3 were functionally classified under categories of vascular development (p = 4.45E-8, correlation significance) and angiogenesis (p = 1.66E-6). Sox18, a known transcriptional regulator of blood vessel formation, shows higher relative gene expression in Id3 WT (1.42 ± 0.417) than Id3 KO (0.332 ± 0.126) adipose tissue. Finally, preliminary findings using pressure myography demonstrate that Id3 KO mice have a higher baseline arterial diameter than Id3 WT. Conclusion: Dysregulation of vascular development during adipose tissue expansion is altering arterial function in an Id3-dependent manner.

Role of transcription factor Ets-1 in the apoptosis of human vascular endothelial cells

2001 ◽  
Vol 188 (2) ◽  
pp. 243-252 ◽  
Author(s):  
Kazuhide Teruyama ◽  
Mayumi Abe ◽  
Toru Nakano ◽  
Chika Iwasaka-Yagi ◽  
Shoki Takahashi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Transcription Factor ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial

Abstract 174: Lacking Gata2 in Endothelial Cells Induces Apoptosis During Vascular Development

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Chih-Wen Ni ◽  
Tom Smith ◽  
Nathan D Lawson
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Development ◽  
Zinc Finger Nucleases ◽  
Positive Staining ◽  
Vascular Endothelial ◽  
Apoptotic Protein ◽  
Flow Circulation ◽  
Media Layer

Gata2 is a transcription factor implicated in hematopoietic development. Previously, we utilized zinc-finger nucleases to generate a zebrafish mutant in gata2a, which reveals a novel role for this gene in vascular development. In particular, gata2a mutant embryos exhibit defects in blood flow circulation due to the formation of shunts within trunk blood vessels, although artery and vein identity appears normal. Here, we show that endothelial cells in gata2a mutant embryos specifically undergo apoptosis as revealed by positive staining of activated caspase-3 at 30hpf but not 24hpf. This endothelial apoptosis can be rescued by re-constitution of gata2a or overexpression of a well-known anti-apoptotic protein, bcl2l1. Interestingly, knocking-down p53 has no effect on the rescue of apoptosis in gata2a mutants, suggesting a p53 independent pathway of apoptosis. Furthermore, we find that mouse retinal vascular endothelial cells lacking gata2 also appear to undergo apoptosis, which prevent angiogenic sprouting from the superficial to media layer of retina vasculature. These findings reveal a new role of gata2 in vascular development whereby gata2 retains an anti-apoptotic function in endothelial cells.

scholarly journals Dual Role of Jam3b in Early Hematopoietic and Vascular Development

2019 ◽  
Author(s):  
Isao Kobayashi ◽  
Jingjing Kobayashi-Sun ◽  
Yuto Hirakawa ◽  
Madoka Ouchi ◽  
Koyuki Yasuda ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Fate ◽  
Molecular Mechanisms ◽  
Vascular Endothelial Cells ◽  
Vascular Development ◽  
Signaling Cascade ◽  
Vascular Endothelial ◽  
Lateral Plate ◽  
Hematopoietic Stem

AbstractIn order to efficiently derive hematopoietic stem cells (HSCs) from pluripotent precursors, it is crucial to understand how mesodermal cells acquire hematopoietic or endothelial identity due to their close developmental connection. Although Npas4 has been recently identified as a conserved master regulator of hemato-vascular development, the molecular mechanisms underlying the cell fate divergence between hematopoietic and vascular endothelial cells are still unclear. Here, we show in zebrafish that the divergence of hematopoietic and vascular endothelial cells in mesodermal cells is regulated by Junctional adhesion molecule 3b (Jam3b) via two independent signaling pathways. Mutation of jam3b led to the reduction of npas4l expression in the posterior lateral plate mesoderm and defect of both hematopoietic and vascular development. Mechanistically, we uncover that Jam3b promotes endothelial specification by regulating npas4l expression through the repression of the Rap1a-Erk signaling cascade. Jam3b subsequently promotes hematopoietic development including HSCs by regulating lrrc15 expression in endothelial precursors through the activation of an integrin-dependent signaling cascade. Our data provide insight into the divergent mechanisms for instructing hematopoietic or vascular fates from mesodermal cells.

Nanofiber-mediated microRNA-126 delivery to vascular endothelial cells for blood vessel regeneration

2016 ◽  
Vol 43 ◽  
pp. 303-313 ◽  
Author(s):  
Fang Zhou ◽  
Xiaoling Jia ◽  
Yang Yang ◽  
Qingmao Yang ◽  
Chao Gao ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Vessel ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Vessel Regeneration
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