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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 2022) | Viewed by 33402

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Dr. Béatrice Charreau

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Centre de Recherche en Transplantation et Immunologie (CRTI) INSERM UMR1064, Université de Nantes, 44093 Nantes, France
Interests: endothelial cell biology; transplantation immunology; innate immunity; CD8 T cells; infection; HCMV; inflammation; cell signaling; biomarkers; MHC; antibodies
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Dear Colleagues,

At the interface between the blood and tissues, the endothelium lining blood vessels is a gatekeeper of vascular barrier integrity that ensures adequate tissue homeostasis and cell trafficking. Consequently, endothelial cells (ECs) display a large panel of key regulatory functions to control vascular tone, blood coagulation and fibrinolysis, complement activation, leucocyte migration, inflammation, and innate and adaptive immunity. These functions result from the fine-tuned expression of specific surface molecules as well as the release of soluble mediators. Transient EC activation may occur after a perturbation, such as an inflammatory stimulus, and is characterized by the acquisition of new cellular functions to restore homeostasis. The activation of the NF-κB, PI3K, and MAPK pathways plays a role in both the tightly controlled transcription of the genes that feature the activated EC phenotype and functions and the return to a resting state. The characteristics and functions of ECs may vary according to the nature of the vessel and tissue, reflecting the heterogeneity of ECs. ECs display selective and bidirectional crosstalks with other cell types, including hematopoietic and immune cells, that influence cell differentiation, activation, and migration. For instance, the TGFβ and Notch signaling pathways are key players orchestrating the bidirectional interplay between ECs and macrophages involved in macrophage polarization, endothelial-to-mesenchymal transition, and graft endothelialization. Endothelial cell-specific biomarkers may provide useful tools for non-invasive investigations of vascular injury in patients. Selective therapeutic approaches targeting ECs are needed to protect ECs from injury, restore vascular integrity, promote re-endothelialization and reparative neoangiogenesis, and, in contrast, avoid excessive proliferation and angiogenesis, such as in tumors. This requires both the identification of endothelium-specific molecular targets and the development of dedicated experimental models for the screening of new drugs or biotherapies.

The main aim of this Special Issue is to provide an overview of recent investigations in the field of endothelial cell biology that advance our understanding of the molecular mechanisms that trigger normal EC functions and dysfunctions in pathologies and demonstrate how better knowledge of EC biology may lead to the discovery of novel molecular diagnostic technologies and targeted therapeutics.

Topics of interest to this Special Issue include, but are not limited to:

endothelial biomarkers for screening and diagnosis;
endothelial targets for immunotherapy;
molecular crosstalks between endothelial cells and other cells;
endothelial cell biology and immunity;
mediators of endothelial cell dysfunction;
molecular markers of endothelial cell heterogeneity;
endothelial cell signaling in cell communication;
endothelial cells as cell targets for drug design;
transcriptomics, epigenomics, and metabolomics in endothelial cells;
non-coding RNAs in endothelial cells;
endothelial cells and virus receptors;
molecular determinants of endothelial cell plasticity; and
shedding of endothelial proteins and release of extracellular vesicles.

Dr. Béatrice Charreau
Guest Editor

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Keywords

angiogenesis
apoptosis
biomarkers
cellular communication
drug screening
endothelial cells
endothelial dysfunction
endothelium targeted therapy
immunity
inflammation
intracellular signaling
molecular diagnostics
Notch signaling
non-coding RNAs
omics
receptor molecules
signaling pathways
SNP genotyping
vascular disorders
therapeutic targets

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Related Special Issues

Advances in Endothelial Cell Biology in International Journal of Molecular Sciences (20 articles)
Advances in Endothelial Cell Biology 3.0 in International Journal of Molecular Sciences (3 articles)

Published Papers (8 papers)

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Research

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11 pages, 1667 KiB

Open AccessArticle

The Interplay between Aquaporin-1 and the Hypoxia-Inducible Factor 1α in a Lipopolysaccharide-Induced Lung Injury Model in Human Pulmonary Microvascular Endothelial Cells

by Chrysi Keskinidou, Nikolaos S. Lotsios, Alice G. Vassiliou, Ioanna Dimopoulou, Anastasia Kotanidou and Stylianos E. Orfanos

Int. J. Mol. Sci. 2022, 23(18), 10588; https://doi.org/10.3390/ijms231810588 - 13 Sep 2022

Cited by 8 | Viewed by 1912

Abstract

Aquaporin-1 (AQP1), a water channel, and the hypoxia-inducible factor 1α (HIF1A) are implicated in acute lung injury responses, modulating among others pulmonary vascular leakage. We hypothesized that the AQP1 and HIF1A systems interact, affecting mRNA, protein levels and function of AQP1 in human pulmonary microvascular endothelial cells (HPMECs) exposed to lipopolysaccharide (LPS). Moreover, the role of AQP1 in apoptosis and wound healing progression was examined. Both AQP1 mRNA and protein expression levels were higher in HPMECs exposed to LPS compared to untreated HPMECs. However, in the LPS-exposed HIF1A-silenced cells, the mRNA and protein expression levels of AQP1 remained unaltered. In the permeability experiments, a statistically significant volume increase was observed at the 360 s time-point in the LPS-exposed HPMECs, while LPS-exposed HIF1A-silenced HPMECs did not exhibit cell swelling, implying a dysfunctional AQP1. AQP1 did not seem to affect cell apoptosis yet could interfere with endothelial migration and/or proliferation. Based on our results, it seems that HIF1A silencing negatively affects AQP1 mRNA and protein expression, as well as AQP1 function, in the setting of lung injury. Full article

(This article belongs to the Special Issue Advances in Endothelial Cell Biology 2.0)

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21 pages, 5628 KiB

Open AccessArticle

Tuning of Liver Sieve: The Interplay between Actin and Myosin Regulatory Light Chain Regulates Fenestration Size and Number in Murine Liver Sinusoidal Endothelial Cells

by Bartlomiej Zapotoczny, Karolina Szafranska, Malgorzata Lekka, Balpreet Singh Ahluwalia and Peter McCourt

Int. J. Mol. Sci. 2022, 23(17), 9850; https://doi.org/10.3390/ijms23179850 - 30 Aug 2022

Cited by 8 | Viewed by 2426

Abstract

Liver sinusoidal endothelial cells (LSECs) facilitate the efficient transport of macromolecules and solutes between the blood and hepatocytes. The efficiency of this transport is realized via transcellular nanopores, called fenestrations. The mean fenestration size is 140 ± 20 nm, with the range from 50 nm to 350 nm being mostly below the limits of diffraction of visible light. The cellular mechanisms controlling fenestrations are still poorly understood. In this study, we tested a hypothesis that both Rho kinase (ROCK) and myosin light chain (MLC) kinase (MLCK)-dependent phosphorylation of MLC regulates fenestrations. We verified the hypothesis using a combination of several molecular inhibitors and by applying two high-resolution microscopy modalities: structured illumination microscopy (SIM) and scanning electron microscopy (SEM). We demonstrated precise, dose-dependent, and reversible regulation of the mean fenestration diameter within a wide range from 120 nm to 220 nm and the fine-tuning of the porosity in a range from ~0% up to 12% using the ROCK pathway. Moreover, our findings indicate that MLCK is involved in the formation of new fenestrations—after inhibiting MLCK, closed fenestrations cannot be reopened with other agents. We, therefore, conclude that the Rho-ROCK pathway is responsible for the control of the fenestration diameter, while the inhibition of MLCK prevents the formation of new fenestrations. Full article

(This article belongs to the Special Issue Advances in Endothelial Cell Biology 2.0)

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18 pages, 2866 KiB

Open AccessArticle

Impact of DICER1 and DROSHA on the Angiogenic Capacity of Human Endothelial Cells

by Heike Braun, Michael Hauke, Anne Ripperger, Christian Ihling, Matthew Fuszard, Robert Eckenstaler and Ralf A. Benndorf

Int. J. Mol. Sci. 2021, 22(18), 9855; https://doi.org/10.3390/ijms22189855 - 12 Sep 2021

Cited by 3 | Viewed by 2444

Abstract

RNAi-mediated knockdown of DICER1 and DROSHA, enzymes critically involved in miRNA biogenesis, has been postulated to affect the homeostasis and the angiogenic capacity of human endothelial cells. To re-evaluate this issue, we reduced the expression of DICER1 or DROSHA by RNAi-mediated knockdown and subsequently investigated the effect of these interventions on the angiogenic capacity of human umbilical vein endothelial cells (HUVEC) in vitro (proliferation, migration, tube formation, endothelial cell spheroid sprouting) and in a HUVEC xenograft assay in immune incompetent NSG^TM mice in vivo. In contrast to previous reports, neither knockdown of DICER1 nor knockdown of DROSHA profoundly affected migration or tube formation of HUVEC or the angiogenic capacity of HUVEC in vivo. Furthermore, knockdown of DICER1 and the combined knockdown of DICER1 and DROSHA tended to increase VEGF-induced BrdU incorporation and induced angiogenic sprouting from HUVEC spheroids. Consistent with these observations, global proteomic analyses showed that knockdown of DICER1 or DROSHA only moderately altered HUVEC protein expression profiles but additively reduced, for example, expression of the angiogenesis inhibitor thrombospondin-1. In conclusion, global reduction of miRNA biogenesis by knockdown of DICER1 or DROSHA does not inhibit the angiogenic capacity of HUVEC. Further studies are therefore needed to elucidate the influence of these enzymes in the context of human endothelial cell-related angiogenesis. Full article

(This article belongs to the Special Issue Advances in Endothelial Cell Biology 2.0)

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Review

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28 pages, 2320 KiB

Open AccessReview

Immune Function of Endothelial Cells: Evolutionary Aspects, Molecular Biology and Role in Atherogenesis

by Stanislav Kotlyarov

Int. J. Mol. Sci. 2022, 23(17), 9770; https://doi.org/10.3390/ijms23179770 - 29 Aug 2022

Cited by 25 | Viewed by 3866

Abstract

Atherosclerosis is one of the key problems of modern medicine, which is due to the high prevalence of atherosclerotic cardiovascular diseases and their significant share in the structure of morbidity and mortality in many countries. Atherogenesis is a complex chain of events that proceeds over many years in the vascular wall with the participation of various cells. Endothelial cells are key participants in vascular function. They demonstrate involvement in the regulation of vascular hemodynamics, metabolism, and innate immunity, which act as leading links in the pathogenesis of atherosclerosis. These endothelial functions have close connections and deep evolutionary roots, a better understanding of which will improve the prospects of early diagnosis and effective treatment. Full article

(This article belongs to the Special Issue Advances in Endothelial Cell Biology 2.0)

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21 pages, 1668 KiB

Open AccessReview

The Interplay of Endothelial P2Y Receptors in Cardiovascular Health: From Vascular Physiology to Pathology

by Cendrine Cabou and Laurent O. Martinez

Int. J. Mol. Sci. 2022, 23(11), 5883; https://doi.org/10.3390/ijms23115883 - 24 May 2022

Cited by 12 | Viewed by 3774

Abstract

The endothelium plays a key role in blood vessel health. At the interface of the blood, it releases several mediators that regulate local processes that protect against the development of cardiovascular disease. In this interplay, there is increasing evidence for a role of extracellular nucleotides and endothelial purinergic P2Y receptors (P2Y-R) in vascular protection. Recent advances have revealed that endothelial P2Y₁-R and P2Y₂-R mediate nitric oxide-dependent vasorelaxation as well as endothelial cell proliferation and migration, which are processes involved in the regeneration of damaged endothelium. However, endothelial P2Y₂-R, and possibly P2Y₁-R, have also been reported to promote vascular inflammation and atheroma development in mouse models, with endothelial P2Y₂-R also being described as promoting vascular remodeling and neointimal hyperplasia. Interestingly, at the interface with lipid metabolism, P2Y₁₂-R has been found to trigger HDL transcytosis through endothelial cells, a process known to be protective against lipid deposition in the vascular wall. Better characterization of the role of purinergic P2Y-R and downstream signaling pathways in determination of the endothelial cell phenotype in healthy and pathological environments has clinical potential for the prevention and treatment of cardiovascular diseases. Full article

(This article belongs to the Special Issue Advances in Endothelial Cell Biology 2.0)

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25 pages, 2447 KiB

Open AccessReview

The Contribution of Gut Microbiota and Endothelial Dysfunction in the Development of Arterial Hypertension in Animal Models and in Humans

by Jessica Maiuolo, Cristina Carresi, Micaela Gliozzi, Rocco Mollace, Federica Scarano, Miriam Scicchitano, Roberta Macrì, Saverio Nucera, Francesca Bosco, Francesca Oppedisano, Stefano Ruga, Anna Rita Coppoletta, Lorenza Guarnieri, Antonio Cardamone, Irene Bava, Vincenzo Musolino, Sara Paone, Ernesto Palma and Vincenzo Mollace

Int. J. Mol. Sci. 2022, 23(7), 3698; https://doi.org/10.3390/ijms23073698 - 28 Mar 2022

Cited by 21 | Viewed by 4957

Abstract

The maintenance of the physiological values of blood pressure is closely related to unchangeable factors (genetic predisposition or pathological alterations) but also to modifiable factors (dietary fat and salt, sedentary lifestyle, overweight, inappropriate combinations of drugs, alcohol abuse, smoking and use of psychogenic substances). Hypertension is usually characterized by the presence of a chronic increase in systemic blood pressure above the threshold value and is an important risk factor for cardiovascular disease, including myocardial infarction, stroke, micro- and macro-vascular diseases. Hypertension is closely related to functional changes in the endothelium, such as an altered production of vasoconstrictive and vasodilator substances, which lead to an increase in vascular resistance. These alterations make the endothelial tissue unresponsive to autocrine and paracrine stimuli, initially determining an adaptive response, which over time lead to an increase in risk or disease. The gut microbiota is composed of a highly diverse bacterial population of approximately 10¹⁴ bacteria. A balanced intestinal microbiota preserves the digestive and absorbent functions of the intestine, protecting from pathogens and toxic metabolites in the circulation and reducing the onset of various diseases. The gut microbiota has been shown to produce unique metabolites potentially important in the generation of hypertension and endothelial dysfunction. This review highlights the close connection between hypertension, endothelial dysfunction and gut microbiota. Full article

(This article belongs to the Special Issue Advances in Endothelial Cell Biology 2.0)

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29 pages, 3418 KiB

Open AccessReview

Organ-Specific Endothelial Cell Differentiation and Impact of Microenvironmental Cues on Endothelial Heterogeneity

by Laia Gifre-Renom, Margo Daems, Aernout Luttun and Elizabeth A. V. Jones

Int. J. Mol. Sci. 2022, 23(3), 1477; https://doi.org/10.3390/ijms23031477 - 27 Jan 2022

Cited by 35 | Viewed by 8231

Abstract

Endothelial cells throughout the body are heterogeneous, and this is tightly linked to the specific functions of organs and tissues. Heterogeneity is already determined from development onwards and ranges from arterial/venous specification to microvascular fate determination in organ-specific differentiation. Acknowledging the different phenotypes of endothelial cells and the implications of this diversity is key for the development of more specialized tissue engineering and vascular repair approaches. However, although novel technologies in transcriptomics and proteomics are facilitating the unraveling of vascular bed-specific endothelial cell signatures, still much research is based on the use of insufficiently specialized endothelial cells. Endothelial cells are not only heterogeneous, but their specialized phenotypes are also dynamic and adapt to changes in their microenvironment. During the last decades, strong collaborations between molecular biology, mechanobiology, and computational disciplines have led to a better understanding of how endothelial cells are modulated by their mechanical and biochemical contexts. Yet, because of the use of insufficiently specialized endothelial cells, there is still a huge lack of knowledge in how tissue-specific biomechanical factors determine organ-specific phenotypes. With this review, we want to put the focus on how organ-specific endothelial cell signatures are determined from development onwards and conditioned by their microenvironments during adulthood. We discuss the latest research performed on endothelial cells, pointing out the important implications of mimicking tissue-specific biomechanical cues in culture. Full article

(This article belongs to the Special Issue Advances in Endothelial Cell Biology 2.0)

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15 pages, 873 KiB

Open AccessReview

The Important Role of Endothelium and Extracellular Vesicles in the Cellular Mechanism of Aortic Aneurysm Formation

by Klaudia Mikołajczyk, Dominika Spyt, Wioletta Zielińska, Agnieszka Żuryń, Inaz Faisal, Murtaz Qamar, Piotr Świniarski, Alina Grzanka and Maciej Gagat

Int. J. Mol. Sci. 2021, 22(23), 13157; https://doi.org/10.3390/ijms222313157 - 6 Dec 2021

Cited by 16 | Viewed by 4065

Abstract

Homeostasis is a fundamental property of biological systems consisting of the ability to maintain a dynamic balance of the environment of biochemical processes. The action of endogenous and exogenous factors can lead to internal balance disorder, which results in the activation of the immune system and the development of inflammatory response. Inflammation determines the disturbances in the structure of the vessel wall, connected with the change in their diameter. These disorders consist of accumulation in the space between the endothelium and the muscle cells of low-density lipoproteins (LDL), resulting in the formation of fatty streaks narrowing the lumen and restricting the blood flow in the area behind the structure. The effect of inflammation may also be pathological dilatation of the vessel wall associated with the development of aneurysms. Described disease entities strongly correlate with the increased migration of immune cells. Recent scientific research indicates the secretion of specific vesicular structures during migration activated by the inflammation. The review focuses on the link between endothelial dysfunction and the inflammatory response and the impact of these processes on the development of disease entities potentially related to the secretion of extracellular vesicles (EVs). Full article

(This article belongs to the Special Issue Advances in Endothelial Cell Biology 2.0)

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