The role of SOX7 transcription factor in early blood vessel development

2018 ◽  
Author(s):  
Ivy Kim Ni Chiang
Keyword(s):  
Transcription Factor ◽  
Blood Vessel ◽  
Blood Vessel Development ◽  
Vessel Development

Role of tissue factor in embryonic blood vessel development

Nature ◽  
1996 ◽  
Vol 383 (6595) ◽  
pp. 73-75 ◽  
Author(s):  
Peter Carmeliet ◽  
Nigel Mackman ◽  
Lieve Moons ◽  
Thomas Luther ◽  
Pierre Gressens ◽  
...  
Keyword(s):  
Blood Vessel ◽  
Tissue Factor ◽  
Blood Vessel Development ◽  
Vessel Development

scholarly journals Activation of Blood Vessel Development in Endometrial Stromal Cells In Vitro Cocultured with Human Peri-Implantation Embryos Revealed by Single-Cell RNA-Seq

Life ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 367
Author(s):  
Bo Lv ◽  
Xiaoyu Xu ◽  
Xunyi Zhang ◽  
Lingbin Qi ◽  
Wen He ◽  
...  
Keyword(s):  
Blood Vessel ◽  
Single Cell ◽  
Stromal Cells ◽  
Differentially Expressed Gene ◽  
Trophoblast Cells ◽  
Endometrial Stromal Cells ◽  
Endometrial Cells ◽  
Blood Vessel Development ◽  
Vessel Development

In humans, the maternal endometrium participates in the physical and physiological interaction with the blastocyst to begin implantation. A bidirectional crosstalk is critical for normal implantation and then a successful pregnancy. While several studies have used animal models or cell lines to study this step, little knowledge was acquired to address the role of endometrial cells in humans. Here, we analyzed single-cell sequencing data from a previous study including 24 non-coculture endometrial stromal cells (EmSCs) and 57 EmSCs after coculture with embryos. We further explored the transcriptomic changes in EmSCs and their interactions with trophoblast cells after coculture. Differentially expressed gene (DEG) analysis showed 1783 upregulated genes and 569 downregulated genes in the cocultured embryos. Weight gene coexpression network and gene ontology analysis of these DEGs showed a higher expression of RAMP1, LTBP1, and LRP1 in EmSCs after coculture, indicating the enrichment of biological processes in blood vessel development and female pregnancy. These data imply that EmSCs start blood vessel development at the implantation stage. Compared with endometrium data in vivo at the implantation window, key pathways including epithelial cell development and oxygen response were involved at this stage. Further analysis using CellphoneDB shed light on the interactions between EmSCs and embryonic trophoblasts, suggesting the important role of integrins and fibroblast growth factor pathways during implantation. Taken together, our work reveals the synchronization signaling and pathways happening at the implantation stage involving the acquisition of receptivity in EmSCs and the interaction between EmSCs and trophoblast cells.

scholarly journals The role of blood flow and microRNAs in blood vessel development

2011 ◽  
Vol 55 (4-5) ◽  
pp. 419-429 ◽  
Author(s):  
Dong Liu ◽  
Janna Krueger ◽  
Ferdinand Le Noble
Keyword(s):  
Blood Flow ◽  
Blood Vessel ◽  
Blood Vessel Development ◽  
Vessel Development

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.

scholarly journals Rab35 Governs Apicobasal Polarity Through Regulation of Actin Dynamics During Sprouting Angiogenesis

2022 ◽  
Author(s):  
Caitlin R Francis ◽  
Hayle Kincross ◽  
Erich J Kushner
Keyword(s):  
Blood Vessel ◽  
Actin Polymerization ◽  
Tissue Type ◽  
Potential Contribution ◽  
Rab Gtpases ◽  
Sprouting Angiogenesis ◽  
Apicobasal Polarity ◽  
Blood Vessel Development ◽  
Vessel Development ◽  
Sprout Formation

In early blood vessel development, trafficking programs, such as those using Rab GTPases, are tasked with delivering vesicular cargo with high spatiotemporal accuracy. However, the function of many Rab trafficking proteins remain ill-defined in endothelial tissue; therefore, their relevance to blood vessel development is unknown. Rab35 has been shown to play an enigmatic role in cellular behaviors which differs greatly between tissue-type and organism. Importantly, Rab35 has never been characterized for its potential contribution in sprouting angiogenesis; thus, our goal was to map Rab35s primary function in angiogenesis. Our results demonstrate that Rab35 is critical for sprout formation; in its absence apicobasal polarity is entirely lost in vitro and in vivo. To determine mechanism, we systematically explored established Rab35 effectors and show that none are operative in endothelial cells. However, we find that Rab35 partners with DENNd1c, an evolutionarily divergent guanine exchange factor, to localize to actin. Here, Rab35 regulates actin polymerization, which is required to setup proper apicobasal polarity during sprout formation. Our findings establish that Rab35 is a potent regulator of actin architecture during blood vessel development.

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