vascular morphogenesis
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Author(s):  
M. Nagameenalochini

Even after the approved classification of congenital vascular tumours/malformations which was first published by Mulliken and Glowacki, in the year 1982, there is still a significant amount of confusion to categorize hemangiomas and vascular malformations. Hemangiomas are considered to be true, benign neoplasms arising from endothelial cells and must be clearly differentiated from localized defects of vascular morphogenesis, i.e., vascular malformations.


2021 ◽  
Author(s):  
Pedro Barbacena ◽  
Maria Dominguez-Cejudo ◽  
Catarina G. Fonseca ◽  
Manuel Gomez-Gonzalez ◽  
Laura M. Faure ◽  
...  

Blood vessel formation generates unique vascular patterns in each individual. The principles governing the apparent stochasticity of this process remain to be elucidated. Using mathematical methods, we find that the transition between two fundamental vascular morphogenetic programs, sprouting angiogenesis and vascular remodeling, is established by a shift on collective front-rear polarity of endothelial cells. We demonstrate that the competition between biochemical (VEGFA) and mechanical (blood flow-induced shear stress) cues controls this collective polarity shift. Shear stress increases tension at focal adhesions overriding VEGFA-driven collective polarization, which relies on tension at adherens junctions. We propose that vascular morphogenetic cues compete to regulate individual cell polarity and migration through tension shifts that translates into tissue-level emergent behaviors, ultimately leading to uniquely organized vascular patterns.


Author(s):  
Anwarul Ferdous ◽  
Sarvjeet Singh ◽  
Yuxuan Luo ◽  
Md J Abedin ◽  
Nan Jiang ◽  
...  

Rationale: Fetal growth and survival depend critically on proper development and integrity of the vascular system. Fli1 (Friend leukemia integration 1), a member of the Ets family of transcription factors, plays critical roles in vascular morphogenesis and homeostasis at mid-gestation, the developmental stage at which expression of its upstream regulator, Etv2, ceases. However, molecular mechanisms of Fli1 action in vascular morphogenesis remain incompletely understood. Objective: To dissect molecular mechanisms of vascular morphogenesis governed by Fli1. Methods and Results: Utilizing Fli1 promoter-driven lineage-specific LacZ expression, Fli1 loss-of-function strategies, and a series of molecular techniques, we demonstrate that Fli1 expression in multipotent myogenic progenitor cells (MPCs) occurs independent of Etv2, and loss of Fli1 expression results in a significant increase in LacZ+ cells in mesoderm within somites and limb buds, leading to reciprocal regulation of the expression of several key endothelial and myogenic genes and vascular abnormalities. Conversely, embryos with conditional Fli1 gain-of-function in MPCs manifested aberrant vasculogenesis with lack of myogenesis. Mechanistically, elevated Fli1 activity in myoblasts and in adult MPCs (also called satellite cells) of X-linked muscular dystrophic mdx mice markedly induced endothelial, but attenuated myogenic, gene expression and differentiation. Importantly, ectopic expression of Myf5 or MyoD, two key myogenic regulators, in Fli1-expressing myoblasts restored their differentiation potential, indicating that levels of Fli1 and myogenic regulators in MPCs inversely regulate their endothelial versus myogenic potential. Conclusions: Fli1 governs vascular morphogenesis by regulating endothelial potential by inversely regulating endothelial versus myogenic programs in MPCs. Our data uncover an important and previously unrecognized mechanism of vascular morphogenesis governed by Fli1 and highlight the physiological significance of the fine tuning of Fli1 activity in multipotent progenitors for proper vascular and muscle morphogenesis during development and disease.


2021 ◽  
Vol 15 ◽  
Author(s):  
Ya-Ting Huang ◽  
Fen-Fang Hong ◽  
Shu-Long Yang

Vascular dementia (VD), a cerebrovascular disease which causes cognitive impairment, is one of the significant factors that affects the quality of senectitude. Atherosclerosis (AS) is a chronic inflammatory syndrome and closely associated with VD. Analyzing the role of AS in VD contribute greatly to its early detection and prevention, but their relationship has not been integrated into a complete network. This review summarizes AS biomarkers as VD predictors for the first time and describes the direct mechanisms of AS causing VD from five aspects: vascular morphogenesis, hemodynamic change, neurovascular unit damage (NVU), oxidative stress, and microRNA (miRNA). Finally, it discriminates the relationship between AS and VD in common risk factors which can be disease or some molecules. In particular, these data imply that the role of AS in VD is not only a pathogenic factor but also a comorbidity in VD. This review aims to bring new ideas for the prediction and treatment of VD.


2021 ◽  
Vol 14 (8) ◽  
pp. e236983
Author(s):  
Kumar Nilesh ◽  
Swenil Shah ◽  
Amol Gautam ◽  
Sagar Thorat

Arteriovenous malformations (AVMs) are rare congenital disorders of vascular morphogenesis. These lesions are characterised by high vascular flow with risk of severe bleeding from accidental trauma or surgical manipulation. Although infrequent, potentially life-threatening and fatal oral bleeding has been reported during extraction of tooth associated with AVM. This paper presents a case of uncontrolled bleeding in an adult female patient undergoing mandibular anterior tooth extraction. The bleeding was related to undiagnosed soft tissue AVM in gingivobuccal space. Management of the case with review of previously reported similar cases is presented.


2021 ◽  
Author(s):  
Tevin CY. Chau ◽  
Sungmin Baek ◽  
Baptiste Coxam ◽  
Renae Skoczylas ◽  
Maria Rondon‐Galeano ◽  
...  

Author(s):  
Dongying Chen ◽  
Martin A. Schwartz ◽  
Michael Simons

Blood vessel acquisition of arterial or venous fate is an adaptive phenomenon in response to increasing blood circulation during vascular morphogenesis. The past two decades of effort in this field led to development of a widely accepted paradigm of molecular regulators centering on VEGF and Notch signaling. More recent findings focused on shear stress-induced cell cycle arrest as a prerequisite for arterial specification substantially modify this traditional understanding. This review aims to summarize key molecular mechanisms that work in concert to drive the acquisition of arterial fate in two distinct developmental settings of vascular morphogenesis: de novo vasculogenesis of the dorsal aorta and postnatal retinal angiogenesis. We will also discuss the questions and conceptual controversies that potentially point to novel directions of investigation and possible clinical relevance.


PLoS Genetics ◽  
2021 ◽  
Vol 17 (6) ◽  
pp. e1009641
Author(s):  
Aurélie Quillien ◽  
Guerric Gilbert ◽  
Manon Boulet ◽  
Séverine Ethuin ◽  
Lucas Waltzer ◽  
...  

During development, the vertebrate vasculature undergoes major growth and remodeling. While the transcriptional cascade underlying blood vessel formation starts to be better characterized, little is known concerning the role and mode of action of epigenetic enzymes during this process. Here, we explored the role of the Protein Arginine Methyl Transferase Prmt5 in blood vessel formation as well as hematopoiesis using zebrafish as a model system. Through the combination of different prmt5 loss-of-function approaches we highlighted a key role of Prmt5 in both processes. Notably, we showed that Prmt5 promotes vascular morphogenesis through the transcriptional control of ETS transcription factors and adhesion proteins in endothelial cells. Interestingly, using a catalytic dead mutant of Prmt5 and a specific drug inhibitor, we found that while Prmt5 methyltransferase activity was required for blood cell formation, it was dispensable for vessel formation. Analyses of chromatin architecture impact on reporter genes expression and chromatin immunoprecipitation experiments led us to propose that Prmt5 regulates transcription by acting as a scaffold protein that facilitates chromatin looping to promote vascular morphogenesis.


2021 ◽  
Author(s):  
Tevin CY Chau ◽  
Sungmin Baek ◽  
Baptiste Coxam ◽  
Renae Skoczylas ◽  
Maria Rondon-Galeano ◽  
...  

Lymphatic vascular development is regulated by well-characterised signalling and transcriptional pathways. These pathways regulate lymphatic endothelial cell (LEC) migration, motility, polarity and and morphogenesis. Canonical and non-canonical WNT signalling pathways are known to control LEC polarity and development of lymphatic vessels and valves. PKD1, encoding Polycystin-1, is the most commonly mutated gene in polycystic kidney disease but has also been shown to be essential in lymphatic vascular morphogenesis. The mechanism by which Pkd1 acts during lymphangiogenesis remains unclear. Here we find that loss of non-canonical WNT signalling components Wnt5a and Ryk phenocopy lymphatic defects seen in Pkd1 knockout mice. To investigate genetic interaction, we generated Pkd1/Wnt5a double knockout mice. Loss of Wnt5a suppressed phenotypes seen in the lymphatic vasculature of Pkd1-/- mice and Pkd1 deletion suppressed phenotypes observed in Wnt5a-/- mice. Thus, we report mutually suppressive roles for Pkd1 and Wnt5a, with developing lymphatic networks restored to a more wild-type state in double mutant mice. This genetic interaction between Pkd1 and the non-canonical WNT signalling pathway ultimately controls LEC polarity and the morphogenesis of developing vessel networks. Our work suggests that Pkd1 acts at least in part by regulating non-canonical WNT signalling during the formation of lymphatic vascular networks.


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