scholarly journals Cell–cell signaling in blood vessel development and function

2018 ◽  
Vol 10 (3) ◽  
Author(s):  
Christer Betsholtz
Keyword(s):  
Blood Vessel ◽  
Cell Signaling ◽  
Blood Vessel Development ◽  
Vessel Development ◽  
And Function ◽  
Cell Cell

scholarly journals Mitochondrial Dynamics: Pathogenesis and Therapeutic Targets of Vascular Diseases

2021 ◽  
Vol 8 ◽  
Author(s):  
Yi Luan ◽  
Kai-Di Ren ◽  
Ying Luan ◽  
Xing Chen ◽  
Yang Yang
Keyword(s):  
Blood Vessel ◽  
Mitochondrial Dynamics ◽  
Vascular Diseases ◽  
Regulatory Mechanisms ◽  
High Morbidity ◽  
The Core ◽  
Blood Vessel Development ◽  
Cell Energy ◽  
Vessel Development ◽  
And Function

Vascular diseases, particularly atherosclerosis, are associated with high morbidity and mortality. Endothelial cell (EC) or vascular smooth muscle cell (VSMC) dysfunction leads to blood vessel abnormalities, which cause a series of vascular diseases. The mitochondria are the core sites of cell energy metabolism and function in blood vessel development and vascular disease pathogenesis. Mitochondrial dynamics, including fusion and fission, affect a variety of physiological or pathological processes. Multiple studies have confirmed the influence of mitochondrial dynamics on vascular diseases. This review discusses the regulatory mechanisms of mitochondrial dynamics, the key proteins that mediate mitochondrial fusion and fission, and their potential effects on ECs and VSMCs. We demonstrated the possibility of mitochondrial dynamics as a potential target for the treatment of vascular diseases.

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.

scholarly journals Defective blood vessel development and pericyte/pvSMC distribution in α4 integrin-deficient mouse embryos

2006 ◽  
Vol 293 (1) ◽  
pp. 165-177 ◽  
Author(s):  
Alison Grazioli ◽  
Christina S. Alves ◽  
Konstantinos Konstantopoulos ◽  
Joy T. Yang
Keyword(s):  
Blood Vessel ◽  
Mouse Embryos ◽  
Deficient Mouse ◽  
Blood Vessel Development ◽  
Vessel Development
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