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Molecular Mechanisms of Endothelial Dysfunction 2.0

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (31 July 2023) | Viewed by 23319

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Dr. Catherine Davis

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Department of Anesthesiology & Perioperative Medicine, Oregon Health & Science University, Portland, OR 97239, USA
Interests: endothelial dysfunction; cerebrovascular disease; JAK-STAT; therapeutic ultrasound
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Dear Colleagues,

A Special Issue on the “Molecular Mechanisms of Endothelial Dysfunction” is being prepared for the journal IJMS. Endothelial cells form a monolayer lining the luminal surface of every blood vessel; however, these cells do much more than simply create a physical barrier between circulating blood and tissues. Endothelial cells are heterogeneous in nature with characteristics depending on vessel size and organ, with highly specialized cells found in the brain and kidney. The endothelium is essential for vascular homeostasis, responding to chemical and physical stimuli in a paracrine, autocrine, and endocrine manner to maintain vasomotor and tissue homeostasis, producing a range of factors that regulate vascular tone, thrombosis, cellular adhesion, inflammation, and smooth muscle proliferation. A functional endothelium and vasculature are essential to tissue health and function.

When endothelial cells become dysfunctional, they lose their ability to maintain homeostasis and gain other properties leading to consequences for both the vessels and the organs they supply. Traditionally, endothelial dysfunction was described as an impaired ability to generate nitric oxide by the endothelium, leading to increased oxidative stress; however, additional markers are now also used depending on organ, such as barrier integrity for cerebrovascular endothelial cells. Endothelial dysfunction may occur as a consequence, as well as contribute to the pathogenesis of many diseases including atherosclerosis, hypertension, type II diabetes, small vessel disease, vascular dementia, Alzheimer’s disease, chronic kidney disease, and stroke, with emerging evidence suggesting that endothelial dysfunction also occurs in complications associated with COVID-19. Endothelial dysfunction is a complex process involving many signaling pathways depending on organ, vessel size, and sex, among other factors.

The elucidation of molecular mechanisms involved in endothelial dysfunction is crucial for the development of efficient therapies to improve endothelial function and vascular homeostasis in disease. This Special Issue invites the submission of original research articles and reviews presenting current studies into the molecular processes in endothelial homeostasis, and how perturbation of these leads to endothelial dysfunction.

Dr. Catherine Davis
Guest Editor

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Keywords

vascular permeability
atherosclerosis
blood brain barrier
endothelial adhesion molecules
vasodilation
thrombosis

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Molecular Mechanisms of Endothelial Dysfunction: Fourth Edition in International Journal of Molecular Sciences (2 articles)

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Research

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15 pages, 5762 KiB

Open AccessArticle

Molecular Mechanisms of Endothelialitis in SARS-CoV-2 Infection: Evidence for VE-Cadherin Cleavage by ACE2

by Laurence Bouillet, Alban Deroux, Meryem Benmarce, Chloé Guérin, Laura Bouvet, Olivia Garnier, Donald K. Martin and Isabelle Vilgrain

Int. J. Mol. Sci. 2023, 24(15), 12525; https://doi.org/10.3390/ijms241512525 - 7 Aug 2023

Cited by 4 | Viewed by 1742

Abstract

Long COVID-19 syndrome appears after Severe Acute Respiratory Syndrome-Corona Virus (SARS-CoV-2) infection with acute damage to microcapillaries, microthrombi, and endothelialitis. However, the mechanisms involved in these processes remain to be elucidated. All blood vessels are lined with a monolayer of endothelial cells called vascular endothelium, which provides a the major function is to prevent coagulation. A component of endothelial cell junctions is VE-cadherin, which is responsible for maintaining the integrity of the vessels through homophilic interactions of its Ca⁺⁺-dependent adhesive extracellular domain. Here we provide the first evidence that VE-cadherin is a target in vitro for ACE2 cleavage because its extracellular domain (hrVE-ED) contains two amino acid sequences for ACE2 substrate recognition at the positions ²⁵⁶P-F²⁵⁷ and ³²¹PMKP-³²⁵L. Indeed, incubation of hrVE-ED with the active ectopeptidase hrACE2 for 16 hrs in the presence of 10 μM ZnCl₂ showed a dose-dependent (from 0.2 ng/μL to 2 ng/μL) decrease of the VE-cadherin immunoreactive band. In vivo, in the blood from patients having severe COVID-19 we detected a circulating form of ACE2 with an apparent molecular mass of 70 kDa, which was barely detectable in patients with mild COVID-19. Of importance, in the patients with severe COVID-19 disease, the presence of three soluble fragments of VE-cadherin (70, 62, 54 kDa) were detected using the antiEC1 antibody while only the 54 kDa fragment was present in patients with mild disease. Altogether, these data clearly support a role for ACE2 to cleave VE-cadherin, which leads to potential biomarkers of SARS-CoV-2 infection related with the vascular disease in “Long COVID-19”. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Endothelial Dysfunction 2.0)

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16 pages, 3017 KiB

Open AccessArticle

Resveratrol Improves Endothelial Function by A PREP1-Mediated Pathway in Mouse Aortic Endothelial Cells

by Serena Cabaro, Ayewa L. Agognon, Cecilia Nigro, Sonia Orso, Immacolata Prevenzano, Alessia Leone, Cristina Morelli, Federica Mormone, Serena Romano, Claudia Miele, Francesco Beguinot, Pietro Formisano and Francesco Oriente

Int. J. Mol. Sci. 2023, 24(15), 11891; https://doi.org/10.3390/ijms241511891 - 25 Jul 2023

Cited by 1 | Viewed by 1308

Abstract

PREP1 is a homeodomain transcription factor that impairs metabolism and is involved in age-related aortic thickening. In this study, we evaluated the role of PREP1 on endothelial function. Mouse Aortic Endothelial Cells (MAECs) transiently transfected with a Prep1 cDNA showed a 1.5- and 1.6-fold increase in eNOS^Thr495 and PKCα phosphorylation, respectively. Proinflammatory cytokines Tnf-α and Il-6 increased by 3.5 and 2.3-fold, respectively, in the presence of Prep1, while the antioxidant genes Sod2 and Atf4 were significantly reduced. Bisindolylmaleimide reverted the effects induced by PREP1, suggesting PKCα to be a mediator of PREP1 action. Interestingly, resveratrol, a phenolic micronutrient compound, reduced the PREP1 levels, eNOS^Thr495, PKCα phosphorylation, and proinflammatory cytokines and increased Sod2 and Atf4 mRNA levels. The experiments performed on the aorta of 18-month-old Prep1 hypomorphic heterozygous mice (Prep1^i/+) expressing low levels of this protein showed a 54 and 60% decrease in PKCα and eNOS^Thr495 phosphorylation and a 45% reduction in Tnf-α levels, with no change in Il-6, compared to same-age WT mice. However, a significant decrease in Sod2 and Atf4 was observed in Prep1^i/+ old mice, indicating the lack of age-induced antioxidant response. These results suggest that Prep1 deficiency partially improved the endothelial function in aged mice and suggested PREP1 as a novel target of resveratrol. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Endothelial Dysfunction 2.0)

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17 pages, 4219 KiB

Open AccessArticle

Growth State-Dependent Activation of eNOS in Response to DHA: Involvement of p38 MAPK

by Shiqi Huang, Carla G. Taylor and Peter Zahradka

Int. J. Mol. Sci. 2023, 24(9), 8346; https://doi.org/10.3390/ijms24098346 - 6 May 2023

Cited by 2 | Viewed by 1685

Abstract

Our laboratory previously reported that docosahexaenoic acid (DHA) differentially activates p38 mitogen-activated protein kinase (MAPK) in growing and quiescent human endothelial cells, which represent the dysfunctional and healthy states in vivo, respectively. Since endothelial nitric oxide synthase (eNOS) activity differs between healthy and dysfunctional endothelial cells, and p38 MAPK reportedly regulates both the activity and expression of eNOS, we hypothesized that the beneficial actions of DHA on endothelial cells are due to eNOS activation by p38 MAPK. The contribution of mitogen- and stress-activated protein kinase (MSK), a p38 MAPK substrate, was also investigated. Growing and quiescent EA.hy926 cells, prepared on Matrigel^®-coated plates, were incubated with inhibitors of p38MAPK or MSK before adding DHA. eNOS phosphorylation and levels were quantified by Western blotting. Treatment with 20 µM DHA activated eNOS in both growth states whereas 125 µM DHA suppressed eNOS activation in growing cells. Quiescent cells had higher basal levels of eNOS than growing cells, while 125 µM DHA decreased eNOS levels in both growth states. p38 MAPK inhibition enhanced eNOS activation in quiescent cells but suppressed it in growing cells. Interestingly, 125 µM DHA counteracted these effects of p38 MAPK inhibition in both growth states. MSK was required for eNOS activation in both growth states, but it only mediated eNOS activation by DHA in quiescent cells. MSK thus affects eNOS via a pathway independent of p38MAPK. Quiescent cells were also more resistant to the apoptosis-inducing effect of 125 µM DHA compared to growing cells. The growth state-dependent regulation of p38MAPK and eNOS by DHA provides novel insight into the molecular mechanisms by which DHA influences endothelial cell function. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Endothelial Dysfunction 2.0)

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18 pages, 3094 KiB

Open AccessArticle

Imbalance of Pulmonary Microvascular Endothelial Cell-Expression of Metalloproteinases and Their Endogenous Inhibitors Promotes Septic Barrier Dysfunction

by Devika P. Jayawardena, Marcello G. Masciantonio, Lefeng Wang, Sanjay Mehta, Natalie DeGurse, Cynthia Pape and Sean E. Gill

Int. J. Mol. Sci. 2023, 24(9), 7875; https://doi.org/10.3390/ijms24097875 - 26 Apr 2023

Cited by 1 | Viewed by 1819

Abstract

Sepsis is a life-threatening disease characterized by excessive inflammation leading to organ dysfunction. During sepsis, pulmonary microvascular endothelial cells (PMVEC) lose barrier function associated with inter-PMVEC junction disruption. Matrix metalloproteinases (MMP) and a disintegrin and metalloproteinases (ADAM), which are regulated by tissue inhibitors of metalloproteinases (TIMPs), can cleave cell–cell junctional proteins, suggesting a role in PMVEC barrier dysfunction. We hypothesize that septic PMVEC barrier dysfunction is due to a disruption in the balance between PMVEC-specific metalloproteinases and TIMPs leading to increased metalloproteinase activity. The effects of sepsis on TIMPs and metalloproteinases were assessed ex vivo in PMVEC from healthy (sham) and septic (cecal ligation and perforation) mice, as well as in vitro in isolated PMVEC stimulated with cytomix, lipopolysaccharide (LPS), and cytomix + LPS vs. PBS. PMVEC had high basal Timp expression and lower metalloproteinase expression, and septic stimulation shifted expression in favour of metalloproteinases. Septic stimulation increased MMP13 and ADAM17 activity associated with a loss of inter-PMVEC junctional proteins and barrier dysfunction, which was rescued by treatment with metalloproteinase inhibitors. Collectively, our studies support a role for metalloproteinase–TIMP imbalance in septic PMVEC barrier dysfunction, and suggest that inhibition of specific metalloproteinases may be a therapeutic avenue for septic patients. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Endothelial Dysfunction 2.0)

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18 pages, 32457 KiB

Open AccessArticle

Altered Storage and Function of von Willebrand Factor in Human Cardiac Microvascular Endothelial Cells Isolated from Recipient Transplant Hearts

by Athinoula Meli, Ann McCormack, Ianina Conte, Qu Chen, James Streetley, Marlene L. Rose, Ruben Bierings, Matthew J. Hannah, Justin E. Molloy, Peter B. Rosenthal and Tom Carter

Int. J. Mol. Sci. 2023, 24(5), 4553; https://doi.org/10.3390/ijms24054553 - 25 Feb 2023

Viewed by 2447

Abstract

The assembly of von Willebrand factor (VWF) into ordered helical tubules within endothelial Weibel–Palade bodies (WPBs) is required for the efficient deployment of the protein at sites of vascular injury. VWF trafficking and storage are sensitive to cellular and environmental stresses that are associated with heart disease and heart failure. Altered storage of VWF manifests as a change in WPB morphology from a rod shape to a rounded shape and is associated with impaired VWF deployment during secretion. In this study, we examined the morphology, ultrastructure, molecular composition and kinetics of exocytosis of WPBs in cardiac microvascular endothelial cells isolated from explanted hearts of patients with a common form of heart failure, dilated cardiomyopathy (DCM; HCMEC_D), or from nominally healthy donors (controls; HCMEC_C). Using fluorescence microscopy, WPBs in HCMEC_C (n = 3 donors) showed the typical rod-shaped morphology containing VWF, P-selectin and tPA. In contrast, WPBs in primary cultures of HCMEC_D (n = 6 donors) were predominantly rounded in shape and lacked tissue plasminogen activator (t-PA). Ultrastructural analysis of HCMEC_D revealed a disordered arrangement of VWF tubules in nascent WPBs emerging from the trans-Golgi network. HCMEC_D WPBs still recruited Rab27A, Rab3B, Myosin-Rab Interacting Protein (MyRIP) and Synaptotagmin-like protein 4a (Slp4-a) and underwent regulated exocytosis with kinetics similar to that seen in HCMECc. However, secreted extracellular VWF strings from HCMEC_D were significantly shorter than for endothelial cells with rod-shaped WPBs, although VWF platelet binding was similar. Our observations suggest that VWF trafficking, storage and haemostatic potential are perturbed in HCMEC from DCM hearts. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Endothelial Dysfunction 2.0)

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14 pages, 3965 KiB

Open AccessCommunication

Endothelial Differentiation of CCM1 Knockout iPSCs Triggers the Establishment of a Specific Gene Expression Signature

by Robin A. Pilz, Dariush Skowronek, Lara Mellinger, Sander Bekeschus, Ute Felbor and Matthias Rath

Int. J. Mol. Sci. 2023, 24(4), 3993; https://doi.org/10.3390/ijms24043993 - 16 Feb 2023

Cited by 1 | Viewed by 2167

Abstract

Cerebral cavernous malformation (CCM) is a neurovascular disease that can lead to seizures and stroke-like symptoms. The familial form is caused by a heterozygous germline mutation in either the CCM1, CCM2, or CCM3 gene. While the importance of a second-hit mechanism in CCM development is well established, it is still unclear whether it immediately triggers CCM development or whether additional external factors are required. We here used RNA sequencing to study differential gene expression in CCM1 knockout induced pluripotent stem cells (CCM1^−/− iPSCs), early mesoderm progenitor cells (eMPCs), and endothelial-like cells (ECs). Notably, CRISPR/Cas9-mediated inactivation of CCM1 led to hardly any gene expression differences in iPSCs and eMPCs. However, after differentiation into ECs, we found the significant deregulation of signaling pathways well known to be involved in CCM pathogenesis. These data suggest that a microenvironment of proangiogenic cytokines and growth factors can trigger the establishment of a characteristic gene expression signature upon CCM1 inactivation. Consequently, CCM1^−/− precursor cells may exist that remain silent until entering the endothelial lineage. Collectively, not only downstream consequences of CCM1 ablation but also supporting factors must be addressed in CCM therapy development. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Endothelial Dysfunction 2.0)

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25 pages, 5624 KiB

Open AccessArticle

Cytochrome P450 1B1 Expression Regulates Intracellular Iron Levels and Oxidative Stress in the Retinal Endothelium

by Yong-Seok Song, Ismail S. Zaitoun, Shoujian Wang, Soesiawati R. Darjatmoko, Christine M. Sorenson and Nader Sheibani

Int. J. Mol. Sci. 2023, 24(3), 2420; https://doi.org/10.3390/ijms24032420 - 26 Jan 2023

Cited by 2 | Viewed by 2354

Abstract

Cytochrome P450 (CYP) 1B1 is a heme-containing monooxygenase found mainly in extrahepatic tissues, including the retina. CYP1B1 substrates include exogenous aromatic hydrocarbons, such as dioxins, and endogenous bioactive compounds, including 17β-estradiol (E2) and arachidonic acid. The endogenous compounds and their metabolites are mediators of various cellular and physiological processes, suggesting that CYP1B1 activity is likely important in maintaining proper cellular and tissue functions. We previously demonstrated that lack of CYP1B1 expression and activity are associated with increased levels of reactive oxygen species and oxidative stress in the retinal vasculature and vascular cells, including retinal endothelial cells (ECs). However, the detailed mechanism(s) of how CYP1B1 activity modulates redox homeostasis remained unknown. We hypothesized that CYP1B1 metabolism of E2 affects bone morphogenic protein 6 (BMP6)-hepcidin-mediated iron homeostasis and lipid peroxidation impacting cellular redox state. Here, we demonstrate retinal EC prepared from Cyp1b1-deficient (Cyp1b1^−/−) mice exhibits increased estrogen receptor-α (ERα) activity and expresses higher levels of BMP6. BMP6 is an inducer of the iron-regulatory hormone hepcidin in the endothelium. Increased hepcidin expression in Cyp1b1^−/− retinal EC resulted in decreased levels of the iron exporter protein ferroportin and, as a result, increased intracellular iron accumulation. Removal of excess iron or antagonism of ERα in Cyp1b1^−/− retinal EC was sufficient to mitigate increased lipid peroxidation and reduce oxidative stress. Suppression of lipid peroxidation and antagonism of ERα also restored ischemia-mediated retinal neovascularization in Cyp1b1^−/− mice. Thus, CYP1B1 expression in retinal EC is important in the regulation of intracellular iron levels, with a significant impact on ocular redox homeostasis and oxidative stress through modulation of the ERα/BMP6/hepcidin axis. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Endothelial Dysfunction 2.0)

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14 pages, 2122 KiB

Open AccessArticle

Endothelial Cell Phenotypes Demonstrate Different Metabolic Patterns and Predict Mortality in Trauma Patients

by Hanne H. Henriksen, Igor Marín de Mas, Lars K. Nielsen, Joseph Krocker, Jakob Stensballe, Sigurður T. Karvelsson, Niels H. Secher, Óttar Rolfsson, Charles E. Wade and Pär I. Johansson

Int. J. Mol. Sci. 2023, 24(3), 2257; https://doi.org/10.3390/ijms24032257 - 23 Jan 2023

Cited by 4 | Viewed by 2212

Abstract

In trauma patients, shock-induced endotheliopathy (SHINE) is associated with a poor prognosis. We have previously identified four metabolic phenotypes in a small cohort of trauma patients (N = 20) and displayed the intracellular metabolic profile of the endothelial cell by integrating quantified plasma metabolomic profiles into a genome-scale metabolic model (iEC-GEM). A retrospective observational study of 99 trauma patients admitted to a Level 1 Trauma Center. Mass spectrometry was conducted on admission samples of plasma metabolites. Quantified metabolites were analyzed by computational network analysis of the iEC-GEM. Four plasma metabolic phenotypes (A–D) were identified, of which phenotype D was associated with an increased injury severity score (p < 0.001); 90% (91.6%) of the patients who died within 72 h possessed this phenotype. The inferred EC metabolic patterns were found to be different between phenotype A and D. Phenotype D was unable to maintain adequate redox homeostasis. We confirm that trauma patients presented four metabolic phenotypes at admission. Phenotype D was associated with increased mortality. Different EC metabolic patterns were identified between phenotypes A and D, and the inability to maintain adequate redox balance may be linked to the high mortality. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Endothelial Dysfunction 2.0)

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Review

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12 pages, 819 KiB

Open AccessReview

Endothelial Dysfunction in Diabetes Mellitus: New Insights

by Michal Dubsky, Jiri Veleba, Dominika Sojakova, Natalia Marhefkova, Vladimira Fejfarova and Edward B. Jude

Int. J. Mol. Sci. 2023, 24(13), 10705; https://doi.org/10.3390/ijms241310705 - 27 Jun 2023

Cited by 13 | Viewed by 3367

Abstract

Endothelial dysfunction (ED) is an important marker of future atherosclerosis and cardiovascular disease, especially in people with diabetes. This article summarizes the evidence on endothelial dysfunction in people with diabetes and adds different perspectives that can affect the presence and severity of ED and its consequences. We highlight that data on ED in type 1 diabetes are lacking and discuss the relationship between ED and arterial stiffness. Several interesting studies have been published showing that ED modulates microRNA, microvesicles, lipid levels, and the endoplasmatic reticulum. A better understanding of ED could provide important insights into the microvascular complications of diabetes, their treatment, and even their prevention. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Endothelial Dysfunction 2.0)

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13 pages, 4786 KiB

Open AccessReview

Dialogue between VE-Cadherin and Sphingosine 1 Phosphate Receptor1 (S1PR1) for Protecting Endothelial Functions

by Olivia Garnier and Isabelle Vilgrain

Int. J. Mol. Sci. 2023, 24(4), 4018; https://doi.org/10.3390/ijms24044018 - 16 Feb 2023

Cited by 2 | Viewed by 2562

Abstract

The endothelial cells (EC) of established blood vessels in adults remain extraordinarily quiescent in the sense that they are not actively proliferating, but they fulfill the necessary role to control the permeability of their monolayer that lines the interior of blood vessels. The cell–cell junctions between ECs in the endothelium comprise tight junctions and adherens homotypic junctions, which are ubiquitous along the vascular tree. Adherens junctions are adhesive intercellular contacts that are crucial for the organization of the EC monolayer and its maintenance and regulation of normal microvascular function. The molecular components and underlying signaling pathways that control the association of adherens junctions have been described in the last few years. In contrast, the role that dysfunction of these adherens junctions has in contributing to human vascular disease remains an important open issue. Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid mediator found at high concentrations in blood which has important roles in the control of the vascular permeability, cell recruitment, and clotting that follow inflammatory processes. This role of S1P is achieved through a signaling pathway mediated through a family of G protein-coupled receptors designated as S1PR1. This review highlights novel evidence for a direct linkage between S1PR1 signaling and the mediation of EC cohesive properties that are controlled by VE-cadherin. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Endothelial Dysfunction 2.0)

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