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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 (30 September 2018) | Viewed by 58697

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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

Dear Colleagues,

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” 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

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Keywords

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

Published Papers (11 papers)

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14 pages, 7905 KiB

Open AccessArticle

Human Brain Endothelial CXCR2 is Inflammation-Inducible and Mediates CXCL5- and CXCL8-Triggered Paraendothelial Barrier Breakdown

by Axel Haarmann, Michael K. Schuhmann, Christine Silwedel, Camelia-Maria Monoranu, Guido Stoll and Mathias Buttmann

Int. J. Mol. Sci. 2019, 20(3), 602; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20030602 - 30 Jan 2019

Cited by 24 | Viewed by 4917

Abstract

Chemokines (C-X-C) motif ligand (CXCL) 5 and 8 are overexpressed in patients with multiple sclerosis, where CXCL5 serum levels were shown to correlate with blood–brain barrier dysfunction as evidenced by gadolinium-enhanced magnetic resonance imaging. Here, we studied the potential role of CXCL5/CXCL8 receptor 2 (CXCR2) as a regulator of paraendothelial brain barrier function, using the well-characterized human cerebral microvascular endothelial cell line hCMEC/D3. Low basal CXCR2 mRNA and protein expression levels in hCMEC/D3 were found to strongly increase under inflammatory conditions. Correspondingly, immunohistochemistry of brain biopsies from two patients with active multiple sclerosis revealed upregulation of endothelial CXCR2 compared to healthy control tissue. Recombinant CXCL5 or CXCL8 rapidly and transiently activated Akt/protein kinase B in hCMEC/D3. This was followed by a redistribution of tight junction-associated protein zonula occludens-1 (ZO-1) and by the formation of actin stress fibers. Functionally, these morphological changes corresponded to a decrease of paracellular barrier function, as measured by a real-time electrical impedance-sensing system. Importantly, preincubation with the selective CXCR2 antagonist SB332235 partially prevented chemokine-induced disturbance of both tight junction morphology and function. We conclude that human brain endothelial CXCR2 may contribute to blood–brain barrier disturbance under inflammatory conditions with increased CXCL5 and CXCL8 expression, where CXCR2 may also represent a novel pharmacological target for blood–brain barrier stabilization. Full article

(This article belongs to the Special Issue Vascular Endothelial Cells)

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18 pages, 4387 KiB

Open AccessArticle

NFκB Inhibition Mitigates Serum Amyloid A-Induced Pro-Atherogenic Responses in Endothelial Cells and Leukocyte Adhesion and Adverse Changes to Endothelium Function in Isolated Aorta

by Abigail Vallejo, Belal Chami, Joanne M. Dennis, Martin Simone, Gulfam Ahmad, Adrian I. Abdo, Arpeeta Sharma, Waled A. Shihata, Nathan Martin, Jaye P. F. Chin-Dusting, Judy B. De Haan and Paul K. Witting

Int. J. Mol. Sci. 2019, 20(1), 105; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20010105 - 28 Dec 2018

Cited by 9 | Viewed by 4795

Abstract

The acute phase protein serum amyloid A (SAA) is associated with endothelial dysfunction and early-stage atherogenesis. Stimulation of vascular cells with SAA increases gene expression of pro-inflammation cytokines and tissue factor (TF). Activation of the transcription factor, nuclear factor kappa-B (NFκB), may be central to SAA-mediated endothelial cell inflammation, dysfunction and pro-thrombotic responses, while targeting NFκB with a pharmacologic inhibitor, BAY11-7082, may mitigate SAA activity. Human carotid artery endothelial cells (HCtAEC) were pre-incubated (1.5 h) with 10 μM BAY11-7082 or vehicle (control) followed by SAA (10 μg/mL; 4.5 h). Under these conditions gene expression for TF and Tumor Necrosis Factor (TNF) increased in SAA-treated HCtAEC and pre-treatment with BAY11-7082 significantly (TNF) and marginally (TF) reduced mRNA expression. Intracellular TNF and interleukin 6 (IL-6) protein also increased in HCtAEC supplemented with SAA and this expression was inhibited by BAY11-7082. Supplemented BAY11-7082 also significantly decreased SAA-mediated leukocyte adhesion to apolipoprotein E-deficient mouse aorta in ex vivo vascular flow studies. In vascular function studies, isolated aortic rings pre-treated with BAY11-7082 prior to incubation with SAA showed improved endothelium-dependent vasorelaxation and increased vascular cyclic guanosine monophosphate (cGMP) content. Together these data suggest that inhibition of NFκB activation may protect endothelial function by inhibiting the pro-inflammatory and pro-thrombotic activities of SAA. Full article

(This article belongs to the Special Issue Vascular Endothelial Cells)

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14 pages, 3226 KiB

Open AccessArticle

Endogenous Ovarian Angiogenesis in Polycystic Ovary Syndrome-Like Rats Induced by Low-Frequency Electro-Acupuncture: The CLARITY Three-Dimensional Approach

by Tong Ma, Peng Cui, Xiaoyu Tong, Wei Hu, Linus R. Shao, Feifei Zhang, Xin Li and Yi Feng

Int. J. Mol. Sci. 2018, 19(11), 3500; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms19113500 - 07 Nov 2018

Cited by 20 | Viewed by 6505

Abstract

We sought to determine the role of ovarian vascularity and neo-angiogenesis in the development of mature follicles in polycystic ovary syndrome (PCOS) and to identify any changes induced by low-frequency electro-acupuncture (EA). Twenty-eight 21-day-old female Wistar rats were randomly divided into four groups—Control, Obesity, PCOS-like, and PCOS-like-EA (n = 7/group). Rats in the Obesity group were fed a high-fat diet throughout the experiment. Rats in the PCOS-like and PCOS-like-EA groups were implanted with a sustained-release tube containing 5α-dihydrotestosterone (DHT) beneath the skin of the neck. Rats in the PCOS-like-EA group received low-frequency EA treatment starting at 70 days for 30 min five times a week for four weeks. At the end of the experiment, all rats were euthanized and perfused with hydrogel. The ovaries were collected for clarification and imaging, and ovarian vascularity and neo-angiogenesis were analyzed. Compared with Control and Obesity rats, the ovaries in DHT-induced PCOS-like rats were smaller in size and had fewer mature follicles and corpora lutea. EA increased angiogenesis in the antral follicles of PCOS-like rats, which in turn promoted follicle maturation, ovulation, and CL formation. Therefore, endogenous ovarian angiogenesis plays a very important role in follicular maturation and might be one of the peripheral and direct mechanisms of EA on PCOS. Full article

(This article belongs to the Special Issue Vascular Endothelial Cells)

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17 pages, 5046 KiB

Open AccessArticle

Endovascular Interventions Permit Isolation of Endothelial Colony-Forming Cells from Peripheral Blood

by Vera Matveeva, Mariam Khanova, Egor Sardin, Larisa Antonova and Olga Barbarash

Int. J. Mol. Sci. 2018, 19(11), 3453; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms19113453 - 02 Nov 2018

Cited by 16 | Viewed by 2866

Abstract

Background: Isolation of endothelial colony-forming cells (ECFCs) is difficult due to the extremely low concentration of their precursors in the peripheral blood (PB). We hypothesized that mechanical injury to the arterial wall during percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) may increase the release of circulating ECFC precursors and induce their growth in vitro. Methods: PB samples from patients with coronary artery disease were collected before, immediately after, and 24 h after the surgery in the CABG group. In the PCI group, PB was isolated before, immediately after the insertion of the catheter, immediately after balloon angioplasty, and 24 h after the PCI. A mononuclear fraction of PB was isolated and differentiated into ECFCs with the following immunophenotyping and evaluation of angiogenic properties. Results. The obtained cultures corresponded to the phenotype and tube forming potential consistent with ECFCs. The isolation of ECFCs in the PCI group was successful in 75% of cases (six out of eight patients) after catheter insertion and in 87.5% (seven out of eight patients) after the balloon inflation and stent deployment. These cultures had high/medium proliferative activity in contrast to those obtained before or 24 h after the intervention. Conclusions: Mechanical injury during PCI increases the release of ECFC precursors to the PB and, hence, the efficacy of ECFC isolation. Full article

(This article belongs to the Special Issue Vascular Endothelial Cells)

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13 pages, 2890 KiB

Open AccessArticle

Copper(II) Bis(diethyldithiocarbamate) Induces the Expression of Syndecan-4, a Transmembrane Heparan Sulfate Proteoglycan, via p38 MAPK Activation in Vascular Endothelial Cells

by Takato Hara, Hiroko Tatsuishi, Tomomi Banno, Tomoya Fujie, Chika Yamamoto, Hiroshi Naka and Toshiyuki Kaji

Int. J. Mol. Sci. 2018, 19(11), 3302; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms19113302 - 24 Oct 2018

Cited by 17 | Viewed by 3562

Abstract

Proteoglycans synthesized by vascular endothelial cells are important for regulating cell function and the blood coagulation-fibrinolytic system. Since we recently reported that copper(II) bis(diethyldithiocarbamate) (Cu(edtc)₂) modulates the expression of some molecules involving the antioxidant and blood coagulation systems, we hypothesized that Cu(edtc)₂ may regulate the expression of proteoglycans and examined this hypothesis using a bovine aortic endothelial cell culture system. The experiments showed that Cu(edtc)₂ induced the expression of syndecan-4, a transmembrane heparan sulfate proteoglycan, in a dose- and time-dependent manner. This induction required the whole structure of Cu(edtc)₂—the specific combination of intramolecular copper and a diethyldithiocarbamate structure—as the ligand. Additionally, the syndecan-4 induction by Cu(edtc)₂ depended on the activation of p38 mitogen-activated protein kinase (MAPK) but not the Smad2/3, NF-E2-related factor2 (Nrf2), or epidermal growth factor receptor (EGFR) pathways. p38 MAPK may be a key molecule for inducing the expression of syndecan-4 in vascular endothelial cells. Full article

(This article belongs to the Special Issue Vascular Endothelial Cells)

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15 pages, 2536 KiB

Open AccessArticle

A Novel Splice-Site Mutation in VEGFC Is Associated with Congenital Primary Lymphoedema of Gordon

by Noeline Nadarajah, Dörte Schulte, Vivienne McConnell, Silvia Martin-Almedina, Christina Karapouliou, Peter S. Mortimer, Steve Jeffery, Stefan Schulte-Merker, Kristiana Gordon, Sahar Mansour and Pia Ostergaard

Int. J. Mol. Sci. 2018, 19(8), 2259; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms19082259 - 01 Aug 2018

Cited by 12 | Viewed by 4784

Abstract

Lymphedema is characterized by chronic swelling of any body part caused by malfunctioning or obstruction in the lymphatic system. Primary lymphedema is often considered genetic in origin. VEGFC, which is a gene encoding the ligand for the vascular endothelial growth factor receptor 3 (VEGFR3/FLT4) and important for lymph vessel development during lymphangiogenesis, has been associated with a specific subtype of primary lymphedema. Through Sanger sequencing of a proband with bilateral congenital pedal edema resembling Milroy disease, we identified a novel mutation (NM_005429.2; c.361+5G>A) in VEGFC. The mutation induced skipping of exon 2 of VEGFC resulting in a frameshift and the introduction of a premature stop codon (p.Ala50ValfsTer18). The mutation leads to a loss of the entire VEGF-homology domain and the C-terminus. Expression of this Vegfc variant in the zebrafish floorplate showed that the splice-site variant significantly reduces the biological activity of the protein. Our findings confirm that the splice-site variant, c.361+5G>A, causes the primary lymphedema phenotype in the proband. We examine the mutations and clinical phenotypes of the previously reported cases to review the current knowledge in this area. Full article

(This article belongs to the Special Issue Vascular Endothelial Cells)

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Open AccessArticle

Impact of Unsaturated Fatty Acids on Cytokine-Driven Endothelial Cell Dysfunction

by Simon Trommer, Anja Leimert, Michael Bucher and Julia Schumann

Int. J. Mol. Sci. 2017, 18(12), 2739; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms18122739 - 16 Dec 2017

Cited by 10 | Viewed by 3524

Abstract

Polyunsaturated fatty acids (PUFA) are reported to exert prophylactic and acute therapeutic effects in diseases linked to endothelial dysfunction. In the present study, the consequences of a PUFA enrichment of endothelial cells (cell line TIME) on cell viability, expression of the cytokines interleukin-6 (IL-6), interleukin-8 (IL-8), granulocyte-macrophage colony-stimulating factor (GM-CSF), and monocyte chemoattractant protein 1 (MCP-1), synthesis of the adhesion molecules intercellular adhesion molecule 1 (ICAM-1) and vascular adhesion molecule 1 (VCAM-1), and production of the coagulation factors plasminogen activator inhibitor-1 (PAI-1), von Willebrand factor (vWF), and tissue factor (TF) was analyzed in parallel. PUFA of both the n3 and the n6 family were investigated in a physiologically relevant concentration of 15 µM, and experiments were performed in both the presence and the absence of the pro-inflammatory cytokines interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ). Supplementation of the culture medium with particular fatty acids was found to have a promoting effect on cellular production of the cytokines IL-6, IL-8, GM-CSF, and MCP-1. Further on, PUFA treatment in the absence of a stimulant diminished the percentage of endothelial cells positive for ICAM-1, and adversely affected the stimulation-induced upregulation of VCAM-1. Cell viability and production of coagulation factors were not or only marginally affected by supplemented fatty acids. Altogether, the data indicate that PUFA of either family are only partially able to counterbalance the destructive consequences of an endothelial dysfunction. Full article

(This article belongs to the Special Issue Vascular Endothelial Cells)

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Review

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12 pages, 554 KiB

Open AccessReview

Vascular Dysfunction Induced by Mercury Exposure

by Tetsuya Takahashi and Takayoshi Shimohata

Int. J. Mol. Sci. 2019, 20(10), 2435; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20102435 - 16 May 2019

Cited by 28 | Viewed by 4847

Abstract

Methylmercury (MeHg) causes severe damage to the central nervous system, and there is increasing evidence of the association between MeHg exposure and vascular dysfunction, hemorrhage, and edema in the brain, but not in other organs of patients with acute MeHg intoxication. These observations suggest that MeHg possibly causes blood–brain barrier (BBB) damage. MeHg penetrates the BBB into the brain parenchyma via active transport systems, mainly the l-type amino acid transporter 1, on endothelial cell membranes. Recently, exposure to mercury has significantly increased. Numerous reports suggest that long-term low-level MeHg exposure can impair endothelial function and increase the risks of cardiovascular disease. The most widely reported mechanism of MeHg toxicity is oxidative stress and related pathways, such as neuroinflammation. BBB dysfunction has been suggested by both in vitro and in vivo models of MeHg intoxication. Therapy targeted at both maintaining the BBB and suppressing oxidative stress may represent a promising therapeutic strategy for MeHg intoxication. This paper reviews studies on the relationship between MeHg exposure and vascular dysfunction, with a special emphasis on the BBB. Full article

(This article belongs to the Special Issue Vascular Endothelial Cells)

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24 pages, 1046 KiB

Open AccessReview

The Contribution of Homocysteine Metabolism Disruption to Endothelial Dysfunction: State-of-the-Art

by Ruben Esse, Madalena Barroso, Isabel Tavares de Almeida and Rita Castro

Int. J. Mol. Sci. 2019, 20(4), 867; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20040867 - 17 Feb 2019

Cited by 173 | Viewed by 11462

Abstract

Homocysteine (Hcy) is a sulfur-containing non-proteinogenic amino acid formed during the metabolism of the essential amino acid methionine. Hcy is considered a risk factor for atherosclerosis and cardiovascular disease (CVD), but the molecular basis of these associations remains elusive. The impairment of endothelial function, a key initial event in the setting of atherosclerosis and CVD, is recurrently observed in hyperhomocysteinemia (HHcy). Various observations may explain the vascular toxicity associated with HHcy. For instance, Hcy interferes with the production of nitric oxide (NO), a gaseous master regulator of endothelial homeostasis. Moreover, Hcy deregulates the signaling pathways associated with another essential endothelial gasotransmitter: hydrogen sulfide. Hcy also mediates the loss of critical endothelial antioxidant systems and increases the intracellular concentration of reactive oxygen species (ROS) yielding oxidative stress. ROS disturb lipoprotein metabolism, contributing to the growth of atherosclerotic vascular lesions. Moreover, excess Hcy maybe be indirectly incorporated into proteins, a process referred to as protein N-homocysteinylation, inducing vascular damage. Lastly, cellular hypomethylation caused by build-up of S-adenosylhomocysteine (AdoHcy) also contributes to the molecular basis of Hcy-induced vascular toxicity, a mechanism that has merited our attention in particular. AdoHcy is the metabolic precursor of Hcy, which accumulates in the setting of HHcy and is a negative regulator of most cell methyltransferases. In this review, we examine the biosynthesis and catabolism of Hcy and critically revise recent findings linking disruption of this metabolism and endothelial dysfunction, emphasizing the impact of HHcy on endothelial cell methylation status. Full article

(This article belongs to the Special Issue Vascular Endothelial Cells)

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10 pages, 2980 KiB

Open AccessReview

Pathological Process of Prompt Connection between Host and Donor Tissue Vasculature Causing Rapid Perfusion of the Engineered Donor Tissue after Transplantation

by Sachiko Sekiya, Shunichi Morikawa, Taichi Ezaki and Tatsuya Shimizu

Int. J. Mol. Sci. 2018, 19(12), 4102; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms19124102 - 18 Dec 2018

Cited by 3 | Viewed by 4180

Abstract

The shortage of donors for transplantation therapy is a serious issue worldwide. Tissue engineering is considered a potential solution to this problem. Connection and perfusion in engineered tissues after transplantation is vital for the survival of the transplanted tissue, especially for tissues requiring blood perfusion to receive nutrients, such as the heart. A myocardial cell sheet containing an endothelial cell network structure was fabricated in vitro using cell sheet technology. Transplantation of the three-dimensional (3D) tissue by layering myocardial sheets could ameliorate ischemic heart disease in a rat model. The endothelial cell network in the 3D tissue was able to rapidly connect to host vasculature and begin perfusion within 24 h after transplantation. In this review, we compare and discuss the engineered tissue–host vasculature connection process between tissue engineered constructs with hydrogels and cell sheets by histological analysis. This review provides information that may be useful for further improvements of in vivo engineered tissue vascularization techniques. Full article

(This article belongs to the Special Issue Vascular Endothelial Cells)

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24 pages, 1702 KiB

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The Different Facades of Retinal and Choroidal Endothelial Cells in Response to Hypoxia

by Effat Alizadeh, Parviz Mammadzada and Helder André

Int. J. Mol. Sci. 2018, 19(12), 3846; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms19123846 - 03 Dec 2018

Cited by 29 | Viewed by 6206

Abstract

Ocular angiogenic diseases, such as proliferative diabetic retinopathy and neovascular age-related macular degeneration, are associated with severe loss of vision. These pathologies originate from different vascular beds, retinal and choroidal microvasculatures, respectively. The activation of endothelial cells (EC) plays pivotal roles in angiogenesis, often triggered by oxygen deficiency. Hypoxia-inducible factors in ECs mediate the transcription of multiple angiogenic genes, including the canonical vascular endothelial growth factors. ECs show notable heterogeneity in function, structure, and disease, therefore the understanding of retinal/choroidal ECs (REC; CEC) biochemical and molecular responses to hypoxia may offer key insights into tissue-specific vascular targeting treatments. The aim of this review is to discuss the differences spanning between REC and CEC, with focus on their response to hypoxia, which could provide innovative and sustainable strategies for site specific targeting of ocular neovascularization. Full article

(This article belongs to the Special Issue Vascular Endothelial Cells)

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