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Vascular Endothelial Cells 2.0
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Vascular Endothelial Cells 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 March 2021) | Viewed by 14307

Special Issue Editors

Prof. Dr. Toshiyuki Kaji

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Guest Editor
Department of Environmental Health, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda 278-8510, Japan
Interests: signaling and cell response; transporter; vascular toxicity; extracellular matrix; atherosclerosis; blood coagulation-fibrinolytic system; growth factors; cytokines
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Yasuyuki Fujiwara

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Guest Editor
Department of Environmental Health, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences, Hachioji 192-0392, Japan
Interests: reactive oxygen species; oxidative stress; shear stress; inflammation; adhesion molecule; vascular permeability; vascular morphology; vascular toxicity; apoptosis; vascular disease; atherosclerosis; proliferation; migration; metallothionein
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Vascular endothelial cells cover the luminal surface of blood vessels and regulate the blood coagulation-fibrinolytic system and vascular tone, while also serving as a barrier between the blood and the subendothelial matrix. To accomplish these functions, the cells synthesize and secrete various substances, including von Willebrand factor, tissue factor, coagulation factor VIII, prostacyclin, thrombomodulin, heparan sulfate/dermatan sulfate proteoglycans, plasminogen activators, plasminogen activator inhibitor-1, endothelin, and nitric oxide.

The expression of these substances is regulated by physiological factors such as growth factors and cytokines, although chemical compounds may also be able to modulate their expression. Additionally, there are known and unknown intracellular signal transductions that regulate endothelial cell functions. Since functional damage to vascular endothelial cells can be a cause of vascular disorders such as atherosclerosis and hypertension, studies that explore the risk factors that can lead to the degradation of endothelial cell functions are important.

Based on the scientific information above, this Special Issue “Vascular Endothelial Cells 2.0” will cover a selection of articles from the fields of biology, physiology, pathology, pharmacology, and toxicology that pertain to vascular endothelial cells and their functions.

Prof. Dr. Toshiyuki Kaji
Prof. Dr. Yasuyuki Fujiwara
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • vascular endothelial cell
  • blood coagulation-fibrinolytic system
  • vascular disease
  • angiogenesis
  • vascular permeability
  • inflammation
  • vascular toxicity

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Published Papers (4 papers)

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Research

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19 pages, 10741 KiB  
Article
Sex-Dependent Impairment of Endothelium-Dependent Relaxation in Aorta of Mice with Overexpression of Hyaluronan in Tunica Media
by Karen Axelgaard Lorentzen, Raquel Hernanz, Estéfano Pinilla, Jens Randel Nyengaard, Lise Wogensen and Ulf Simonsen
Int. J. Mol. Sci. 2023, 24(9), 8436; https://doi.org/10.3390/ijms24098436 - 8 May 2023
Viewed by 2156
Abstract
Diabetic macroangiopathy is characterized by increased extracellular matrix deposition, including excessive hyaluronan accumulation, vessel thickening and stiffness, and endothelial dysfunction in large arteries. We hypothesized that the overexpression of hyaluronan in the tunica media also led to endothelial cell (EC) dysfunction. To address [...] Read more.
Diabetic macroangiopathy is characterized by increased extracellular matrix deposition, including excessive hyaluronan accumulation, vessel thickening and stiffness, and endothelial dysfunction in large arteries. We hypothesized that the overexpression of hyaluronan in the tunica media also led to endothelial cell (EC) dysfunction. To address this hypothesis, we investigated the following in the aortas of mice with excessive hyaluronan accumulation in the tunica media (HAS-2) and wild-type mice: EC dysfunction via myograph studies, nitric oxide (NO) bioavailability via diaminofluorescence, superoxide formation via dihydroethidium fluorescence, and the distances between ECs via stereological methods. EC dysfunction, characterized by blunted relaxations in response to acetylcholine and decreased NO bioavailability, was found in the aortas of male HAS-2 mice, while it was unaltered in the aortas of female HAS-2 mice. Superoxide levels increased and extracellular superoxide dismutase (ecSOD) expression decreased in the aortas of male and female HAS-2 mice. The EC–EC distances and LDL receptor expression were markedly increased in the HAS-2 aortas of male mice. Our findings suggest hyaluronan increases oxidative stress in the vascular wall and that together with increased EC distance, it is associated with a sex-specific decrease in NO levels and endothelial dysfunction in the aorta of male HAS-2 transgenic mice. Full article
(This article belongs to the Special Issue Vascular Endothelial Cells 2.0)
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12 pages, 3146 KiB  
Article
Vascular Endothelial Integrity Affects the Severity of Enterovirus-Mediated Cardiomyopathy
by Jin-Ho Park, Ha-Hyeon Shin, Hyun-Seung Rhyu, So-Hee Kim, Eun-Seok Jeon and Byung-Kwan Lim
Int. J. Mol. Sci. 2021, 22(6), 3053; https://doi.org/10.3390/ijms22063053 - 17 Mar 2021
Cited by 7 | Viewed by 2754
Abstract
Coxsackievirus and adenovirus receptor (CAR) is present in epithelial and vascular endothelial cell junctions. We have previously shown a hemorrhagic phenotype in germ-line CAR knock-out mouse embryos; we have also found that CAR interacts with ZO-1 and β-catenin. However, the role of CAR [...] Read more.
Coxsackievirus and adenovirus receptor (CAR) is present in epithelial and vascular endothelial cell junctions. We have previously shown a hemorrhagic phenotype in germ-line CAR knock-out mouse embryos; we have also found that CAR interacts with ZO-1 and β-catenin. However, the role of CAR in vascular endothelial junction permeability has not been proven. To understand the roles of CAR in the vascular endothelial junctions, we generated endothelium-specific CAR knockout (CAR-eKO) mice. In the absence of CAR, the endothelial cell layer showed an increase in transmembrane electrical resistance (TER, Ω) and coxsackievirus permeability. Evans blue dye and 70 kDa dextran-FITC were delivered by tail vein injection. We observed increased vascular permeability in the hearts of adult CAR-eKO mice compare with wild-type (WT) mice. There was a marked increase in monocyte and macrophage penetration into the peritoneal cavity caused by thioglycolate-induced peritonitis. We found that CAR ablation in endothelial cells was not significantly increased coxsackievirus B3 (CVB3) induced myocarditis in murine model. However, tissue virus titers were significantly higher in CAR-eKO mice compared with WT. Moreover, CVB3 was detected in the brain of CAR-eKO mice. Endothelial CAR deletion affects the expression of major endothelial junction proteins, such as cadherin and platelet endothelial cell adhesion molecule-1 (PECAM-1) in the cultured endothelial cells as well as liver vessel. We suggest that CAR expression is required for normal vascular permeability and endothelial tight junction homeostasis. Furthermore, CVB3 organ penetration and myocarditis severities were dependent on the endothelial CAR level. Full article
(This article belongs to the Special Issue Vascular Endothelial Cells 2.0)
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16 pages, 3993 KiB  
Article
Arsenite Inhibits Tissue-Type Plasminogen Activator Synthesis through NRF2 Activation in Cultured Human Vascular Endothelial EA.hy926 Cells
by Tsuyoshi Nakano, Tsutomu Takahashi, Chika Yamamoto, Eiko Yoshida, Toshiyuki Kaji and Yasuyuki Fujiwara
Int. J. Mol. Sci. 2021, 22(2), 739; https://doi.org/10.3390/ijms22020739 - 13 Jan 2021
Cited by 4 | Viewed by 2519
Abstract
Chronic arsenic exposure is known to be related to the progression of atherosclerosis. However, the pathogenic mechanisms of arsenic-induced atherosclerosis have not been fully elucidated. Because disruption of the blood coagulation/fibrinolytic system is involved in the development of arteriosclerosis, we investigated the effect [...] Read more.
Chronic arsenic exposure is known to be related to the progression of atherosclerosis. However, the pathogenic mechanisms of arsenic-induced atherosclerosis have not been fully elucidated. Because disruption of the blood coagulation/fibrinolytic system is involved in the development of arteriosclerosis, we investigated the effect of arsenite on fibrinolytic activity in human vascular endothelial EA.hy926 cells in the present study. Fibrinolysis depends on the balance between tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor 1 (PAI-1) secreted from vascular endothelial cells. We found that arsenite reduced fibrinolytic t-PA activity by inhibiting its synthesis without affecting PAI-1 production. The inhibitory effect of arsenite on t-PA expression was partially recovered by the reactive oxygen species (ROS) scavenger Trolox. The nuclear factor erythroid 2 related factor 2 (NRF2) pathway is known to be activated by arsenite via ROS production. We confirmed that arsenite activated the NRF2 pathway, and arsenite-induced inhibition of fibrinolytic t-PA activity was abrogated in NRF2-knockdown EA.hy926 cells. These results suggest that arsenite inhibits the fibrinolytic activity of t-PA by selectively suppressing its synthesis via activation of the NRF2 pathway in vascular endothelial cells. Full article
(This article belongs to the Special Issue Vascular Endothelial Cells 2.0)
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Review

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25 pages, 3791 KiB  
Review
Endothelial Cells as Tools to Model Tissue Microenvironment in Hypoxia-Dependent Pathologies
by Aleksandra Majewska, Kinga Wilkus, Klaudia Brodaczewska and Claudine Kieda
Int. J. Mol. Sci. 2021, 22(2), 520; https://doi.org/10.3390/ijms22020520 - 7 Jan 2021
Cited by 20 | Viewed by 6154
Abstract
Endothelial cells (ECs) lining the blood vessels are important players in many biological phenomena but are crucial in hypoxia-dependent diseases where their deregulation contributes to pathology. On the other hand, processes mediated by ECs, such as angiogenesis, vessel permeability, interactions with cells and [...] Read more.
Endothelial cells (ECs) lining the blood vessels are important players in many biological phenomena but are crucial in hypoxia-dependent diseases where their deregulation contributes to pathology. On the other hand, processes mediated by ECs, such as angiogenesis, vessel permeability, interactions with cells and factors circulating in the blood, maintain homeostasis of the organism. Understanding the diversity and heterogeneity of ECs in different tissues and during various biological processes is crucial in biomedical research to properly develop our knowledge on many diseases, including cancer. Here, we review the most important aspects related to ECs’ heterogeneity and list the available in vitro tools to study different angiogenesis-related pathologies. We focus on the relationship between functions of ECs and their organo-specificity but also point to how the microenvironment, mainly hypoxia, shapes their activity. We believe that taking into account the specific features of ECs that are relevant to the object of the study (organ or disease state), especially in a simplified in vitro setting, is important to truly depict the biology of endothelium and its consequences. This is possible in many instances with the use of proper in vitro tools as alternative methods to animal testing. Full article
(This article belongs to the Special Issue Vascular Endothelial Cells 2.0)
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