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Cells
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Vascular Endothelial Functions in Health and Diseases
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Vascular Endothelial Functions in Health and Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (20 November 2023) | Viewed by 19590

Special Issue Editors

Dr. Agnes Klar

E-Mail Website
Guest Editor
Tissue Biology Research Unit, Department of Surgery, University Children’s Hospital Zurich, 8032 Zurich, Switzerland
Interests: human skin; keratinocytes; endothelial cells; skin substitutes; stem cells; melanocytes; adipose-dervied stem cells; fat tissue; skin inflammation; immune cells; skin adipocyte progenitors
Special Issues, Collections and Topics in MDPI journals
Dr. Yang Lin

E-Mail Website
Guest Editor
Weill Cornell Medicine, 505 East 70th Street, 1320 York Avenue, New York, NY 10021, USA
Interests: vascular biology; stem cell biology; hematopoiesis

Special Issue Information

Dear Colleagues,

This Special Issue provides a comprehensive review of the rapidly expanding field of vascular biology. The vascular endothelial cell layer separates blood from underlying tissue, thereby exerting multiple functions including control of vascular tone and hemodynamics, participation in blood clotting, modulation of immune reactions, triggering angiogenesis, and exchange of substances between blood and tissues. Therefore, endothelial dysfunction or damage is a cause of several human pathologies such as chronic wounds, cardiovascular diseases, diabetes, cancer, lung and brain injury, and infectious diseases, including COVID-19. Advancement in endothelial protection and correction of endothelial dysfunction requires the identification of the key molecules that participate in signaling cascades, metabolic health, and macromolecule interaction networks in endothelial cells. Some of these molecules are predicted to gain pharmacologic value in emerging vasculoprotective therapies.

Dr. Agnes Klar
Dr. Yang Lin
Guest Editors

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • inflammation
  • angiogenesis
  • vasculogenesis
  • perivascular basement membrane
  • shear stress
  • intracellular signaling
  • transendothelial transport
  • endothelium dysfunction
  • hemodynamic forces
  • immune cell adhesion

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Published Papers (7 papers)

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Research

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15 pages, 2167 KiB  
Article
HDAC6 and ERK/ADAM17 Regulate VEGF-Induced NOTCH Signaling in Lung Endothelial Cells
by Sheng Xia, Heather L. Menden, Sherry M. Mabry and Venkatesh Sampath
Cells 2023, 12(18), 2231; https://doi.org/10.3390/cells12182231 - 8 Sep 2023
Cited by 3 | Viewed by 1386
Abstract
Angiogenesis plays a critical role in various physiological and pathological processes and is regulated by VEGF. Histone Deacetylase 6 (HDAC6) is a class IIB HDAC that regulates cytoplasmic signaling through deacetylation and is emerging as a target for modulating angiogenesis. We investigated the [...] Read more.
Angiogenesis plays a critical role in various physiological and pathological processes and is regulated by VEGF. Histone Deacetylase 6 (HDAC6) is a class IIB HDAC that regulates cytoplasmic signaling through deacetylation and is emerging as a target for modulating angiogenesis. We investigated the hypothesis that VEGF-induced endothelial cell (EC) NOTCH signaling is regulated by HDAC6 through acetylation of NOTCH intracellular cytoplasmic domain (NICD). In pulmonary endothelial cells (EC), VEGF-induced activation of the NICD transcriptional response was regulated by ERK1/2 and ADAM 17 and required DLL4. While HDAC6 inhibition induced the acetylation of NICD and stabilized NICD, it repressed NICD-SNW1 binding required for the NOTCH transcriptional responses. In vitro experiments showed that HDAC6 inhibition inhibited lung EC angiogenesis, and neonatal mice treated with a systemic HDAC6 inhibitor had significantly altered angiogenesis and alveolarization. These findings shed light on the role of HDAC6 in modulating VEGF-induced angiogenesis through acetylation and repression of the transcriptional regulators, NICD and SNW1. Full article
(This article belongs to the Special Issue Vascular Endothelial Functions in Health and Diseases)
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15 pages, 2816 KiB  
Article
Capillary Dynamics Regulate Post-Ischemic Muscle Damage and Regeneration in Experimental Hindlimb Ischemia
by Galina Wirth, Greta Juusola, Santeri Tarvainen, Johanna P. Laakkonen, Petra Korpisalo and Seppo Ylä-Herttuala
Cells 2023, 12(16), 2060; https://doi.org/10.3390/cells12162060 - 14 Aug 2023
Cited by 1 | Viewed by 2929
Abstract
This study aimed to show the significance of capillary function in post-ischemic recovery from the perspective of physiological parameters, such as blood flow, hemoglobin oxygenation and tissue regeneration. Muscle-level microvascular alterations of blood flow and hemoglobin oxygenation, and post-ischemic myofiber and capillary responses [...] Read more.
This study aimed to show the significance of capillary function in post-ischemic recovery from the perspective of physiological parameters, such as blood flow, hemoglobin oxygenation and tissue regeneration. Muscle-level microvascular alterations of blood flow and hemoglobin oxygenation, and post-ischemic myofiber and capillary responses were analyzed in aged, healthy C57Bl/6J mice (n = 48) and aged, hyperlipidemic LDLR−/−ApoB100/100 mice (n = 69) after the induction of acute hindlimb ischemia using contrast ultrasound, photoacoustic imaging and histological analyses, respectively. The capillary responses that led to successful post-ischemic muscle repair in C57Bl/6J mice included an early capillary dilation phase, preceding the return of arterial driving pressure, followed by an increase in capillary density that further supported satellite cell-induced muscle regeneration. Initial capillary enlargement was absent in the LDLR−/−ApoB100/100 mice with lifelong moderate hypercholesterolemia and led to an inability to recover arterial driving pressure, with a resulting increase in distal necrosis, chronic tissue damage and a delay in the overall recovery after ischemia. To conclude, this manuscript highlights, beyond arterial collateralization, the importance of the proper function of the capillary endothelium in post-ischemic recovery and displays how post-ischemic capillary dynamics associate beyond tissue blood flow to both hemoglobin oxygenation and tissue regeneration. Full article
(This article belongs to the Special Issue Vascular Endothelial Functions in Health and Diseases)
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16 pages, 6362 KiB  
Article
Reduced Tie2 in Microvascular Endothelial Cells Is Associated with Organ-Specific Adhesion Molecule Expression in Murine Health and Endotoxemia
by Peter J. Zwiers, Jacqueline P. F. E. Lucas, Rianne M. Jongman, Matijs van Meurs, Eliane R. Popa and Grietje Molema
Cells 2023, 12(14), 1850; https://doi.org/10.3390/cells12141850 - 14 Jul 2023
Cited by 1 | Viewed by 1731
Abstract
Endothelial cells (ECs) in the microvasculature in organs are active participants in the pathophysiology of sepsis. Tyrosine protein kinase receptor Tie2 (Tek; Tunica interna Endothelial cell Kinase) is thought to play a role in their inflammatory response, yet data are inconclusive. We investigated [...] Read more.
Endothelial cells (ECs) in the microvasculature in organs are active participants in the pathophysiology of sepsis. Tyrosine protein kinase receptor Tie2 (Tek; Tunica interna Endothelial cell Kinase) is thought to play a role in their inflammatory response, yet data are inconclusive. We investigated acute endotoxemia-induced changes in the expression of Tie2 and inflammation-associated endothelial adhesion molecules E-selectin and VCAM-1 (vascular cell adhesion molecule-1) in kidneys and lungs in inducible, EC-specific Tie2 knockout mice. The extent of Tie2 knockout in healthy mice differed between microvascular beds, with low to absent expression in arterioles in kidneys and in capillaries in lungs. In kidneys, Tie2 mRNA dropped more than 70% upon challenge with lipopolysaccharide (LPS) in both genotypes, with no change in protein. In renal arterioles, tamoxifen-induced Tie2 knockout was associated with higher VCAM-1 protein expression in healthy conditions. This did not increase further upon challenge of mice with LPS, in contrast to the increased expression occurring in control mice. Also, in lungs, Tie2 mRNA levels dropped within 4 h after LPS challenge in both genotypes, while Tie2 protein levels did not change. In alveolar capillaries, where tamoxifen-induced Tie2 knockout did not affect the basal expression of either adhesion molecule, a 4-fold higher E-selectin protein expression was observed after exposure to LPS compared to controls. The here-revealed heterogeneous effects of absence of Tie2 in ECs in kidney and lung microvasculature in health and in response to acute inflammatory activation calls for further in vivo investigations into the role of Tie2 in EC behavior. Full article
(This article belongs to the Special Issue Vascular Endothelial Functions in Health and Diseases)
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18 pages, 5968 KiB  
Article
Development of an In Vitro Blood Vessel Model Using Autologous Endothelial Cells Generated from Footprint-Free hiPSCs to Analyze Interactions of the Endothelium with Blood Cell Components and Vascular Implants
by Josefin Weber, Marbod Weber, Adrian Feile, Christian Schlensak and Meltem Avci-Adali
Cells 2023, 12(9), 1217; https://doi.org/10.3390/cells12091217 - 22 Apr 2023
Cited by 5 | Viewed by 2213
Abstract
Cardiovascular diseases are the leading cause of death globally. Vascular implants, such as stents, are required to treat arterial stenosis or dilatation. The development of innovative stent materials and coatings, as well as novel preclinical testing strategies, is needed to improve the bio- [...] Read more.
Cardiovascular diseases are the leading cause of death globally. Vascular implants, such as stents, are required to treat arterial stenosis or dilatation. The development of innovative stent materials and coatings, as well as novel preclinical testing strategies, is needed to improve the bio- and hemocompatibility of current stents. In this study, a blood vessel-like polydimethylsiloxane (PDMS) model was established to analyze the interaction of an endothelium with vascular implants, as well as blood-derived cells, in vitro. Using footprint-free human induced pluripotent stem cells (hiPSCs) and subsequent differentiation, functional endothelial cells (ECs) expressing specific markers were generated and used to endothelialize an artificial PDMS lumen. The established model was used to demonstrate the interaction of the created endothelium with blood-derived immune cells, which also allowed for real-time imaging. In addition, a stent was inserted into the endothelialized lumen to analyze the surface endothelialization of stents. In the future, this blood vessel-like model could serve as an in vitro platform to test the influence of vascular implants and coatings on endothelialization and to analyze the interaction of the endothelium with blood cell components. Full article
(This article belongs to the Special Issue Vascular Endothelial Functions in Health and Diseases)
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Review

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27 pages, 1918 KiB  
Review
VEGF—Virus Interactions: Pathogenic Mechanisms and Therapeutic Applications
by Cristina Sánchez-Martínez, Esther Grueso, Tania Calvo-López, Jorge Martinez-Ortega, Ana Ruiz and José M. Almendral
Cells 2024, 13(21), 1815; https://doi.org/10.3390/cells13211815 - 4 Nov 2024
Viewed by 999
Abstract
Many types of viruses directly or indirectly target the vascular endothelial growth factor (VEGF) system, which is a central regulator of vasculogenesis and angiogenesis in physiological homeostasis, causing diverse pathologies. Other viruses have been developed into effective therapeutic tools for VEGF modulation in [...] Read more.
Many types of viruses directly or indirectly target the vascular endothelial growth factor (VEGF) system, which is a central regulator of vasculogenesis and angiogenesis in physiological homeostasis, causing diverse pathologies. Other viruses have been developed into effective therapeutic tools for VEGF modulation in conditions such as cancer and eye diseases. Some viruses may alter the levels of VEGF in the pathogenesis of respiratory syndromes, or they may encode VEGF-like factors, promoting vascular disruption and angiogenesis to enable viruses’ systemic spread. Oncogenic viruses may express interactive factors that perturb VEGF’s functional levels or downstream signaling, which increases the neovascularization and metastasis of tumors. Furthermore, many viruses are being developed as therapeutic vectors for vascular pathologies in clinical trials. Major examples are those viral vectors that inhibit the role of VEGF in the neovascularization required for cancer progression; this is achieved through the induction of immune responses, by exposing specific peptides that block signaling or by expressing anti-VEGF and anti-VEGF receptor-neutralizing antibodies. Other viruses have been engineered into effective pro- or anti-angiogenesis multitarget vectors for neovascular eye diseases, paving the way for therapies with improved safety and minimal side effects. This article critically reviews the large body of literature on these issues, highlighting those contributions that describe the molecular mechanisms, thus expanding our understanding of the VEGF–virus interactions in disease and therapy. This could facilitate the clinical use of therapeutic virus vectors in precision medicine for the VEGF system. Full article
(This article belongs to the Special Issue Vascular Endothelial Functions in Health and Diseases)
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18 pages, 1622 KiB  
Review
Vascular Inflammatory Diseases and Endothelial Phenotypes
by Jenita Immanuel and Sanguk Yun
Cells 2023, 12(12), 1640; https://doi.org/10.3390/cells12121640 - 15 Jun 2023
Cited by 22 | Viewed by 4352
Abstract
The physiological functions of endothelial cells control vascular tone, permeability, inflammation, and angiogenesis, which significantly help to maintain a healthy vascular system. Several cardiovascular diseases are characterized by endothelial cell activation or dysfunction triggered by external stimuli such as disturbed flow, hypoxia, growth [...] Read more.
The physiological functions of endothelial cells control vascular tone, permeability, inflammation, and angiogenesis, which significantly help to maintain a healthy vascular system. Several cardiovascular diseases are characterized by endothelial cell activation or dysfunction triggered by external stimuli such as disturbed flow, hypoxia, growth factors, and cytokines in response to high levels of low-density lipoprotein and cholesterol, hypertension, diabetes, aging, drugs, and smoking. Increasing evidence suggests that uncontrolled proinflammatory signaling and further alteration in endothelial cell phenotypes such as barrier disruption, increased permeability, endothelial to mesenchymal transition (EndMT), and metabolic reprogramming further induce vascular diseases, and multiple studies are focusing on finding the pathways and mechanisms involved in it. This review highlights the main proinflammatory stimuli and their effects on endothelial cell function. In order to provide a rational direction for future research, we also compiled the most recent data regarding the impact of endothelial cell dysfunction on vascular diseases and potential targets that impede the pathogenic process. Full article
(This article belongs to the Special Issue Vascular Endothelial Functions in Health and Diseases)
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15 pages, 1694 KiB  
Review
Endothelial Function in Dyslipidemia: Roles of LDL-Cholesterol, HDL-Cholesterol and Triglycerides
by Yukihito Higashi
Cells 2023, 12(9), 1293; https://doi.org/10.3390/cells12091293 - 1 May 2023
Cited by 26 | Viewed by 4639
Abstract
Dyslipidemia is associated with endothelial dysfunction. Endothelial dysfunction is the initial step for atherosclerosis, resulting in cardiovascular complications. It is clinically important to break the process of endothelial dysfunction to cardiovascular complications in patients with dyslipidemia. Lipid-lowering therapy enables the improvement of endothelial [...] Read more.
Dyslipidemia is associated with endothelial dysfunction. Endothelial dysfunction is the initial step for atherosclerosis, resulting in cardiovascular complications. It is clinically important to break the process of endothelial dysfunction to cardiovascular complications in patients with dyslipidemia. Lipid-lowering therapy enables the improvement of endothelial function in patients with dyslipidemia. It is likely that the relationships of components of a lipid profile such as low-density lipoprotein cholesterol, high-density lipoprotein cholesterol and triglycerides with endothelial function are not simple. In this review, we focus on the roles of components of a lipid profile in endothelial function. Full article
(This article belongs to the Special Issue Vascular Endothelial Functions in Health and Diseases)
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