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Biomolecules
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Regulation of the Endothelial Cell Barrier
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Regulation of the Endothelial Cell Barrier

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Cellular Biochemistry".

Deadline for manuscript submissions: closed (25 February 2024) | Viewed by 20090

Special Issue Editors

Prof. Dr. Carola Yvette Förster

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Guest Editor
Julius-Maximilians-Universitat Wurzburg, Department of Anesthesia and Critical Care, Wurzburg, Germany
Interests: cerebrovascular biology; cardiovascular biology; brain-heart; brain cancer; neuroinflammation; ischemic brain injury; systems biology and mathematical modeling
Special Issues, Collections and Topics in MDPI journals
Dr. Brandon Kim

E-Mail Website
Guest Editor
Department of Biological Sciences, University of Alabama, Tuscaloosa, AL, USA
Interests: host-pathogen interaction between bacterial pathogens and the human blood-brain barrier
Prof. Dr. Sergey Shityakov

E-Mail Website
Guest Editor
Infochemistry Scientific Center, ITMO University, Lomonosova str, 9, Saint-Petersburg 191002, Russia
Interests: blood–brain barrier; molecular modeling; biomedicine

Special Issue Information

Dear Colleagues,

For this Special Issue, we would like to attract contributions on the identification of mechanisms that link endothelial dysfunction to various health issues, such as environmental stress and aging to cardiovascular disease and stroke, thereby supporting the development of novel preventive and therapeutic approaches, including virtual drug screening and mathematical modeling approaches.

Cardiovascular disease (CVD) and stroke are the leading causes of human death worldwide. Coronary artery disease and stroke account for 80% of deaths in males and 75% in females. Together, they were the cause of 17.9 million deaths in 2015 (32.1%), compared with 12.3 million (25.8%) in 1990. From this, it is clear that CVD is one of the most important causes of morbidity and mortality worldwide. The prevalence of CVD increases with age, and, due to this, it is amongst the typical diseases associated with aging; as described by the World Health Organization (WHO), aging can be defined as the progressive loss of cellular functions and the increased mortality of cells over time. In the course of life, the loss of cellular rescue functions and cellular stress response in cellular senescence is linked to the emergence of aging-associated diseases, such as CVD, degeneration, and cancer.

Recent studies in the field of environmental cardiology and neurology suggest that environmental toxins influence CVD and cerebrovascular disease. Extensive evidence even indicates that environmental factors directly contribute to CVD risk and incidence via the resulting endothelial dysfunction. Additionally, CVD and cerebrovascular disease risk is affected by changes in nutritional and lifestyle choices. Exposure to tobacco smoke is paradigmatic of such environmental risk, and is strongly and positively associated with increased cardiovascular morbidity and mortality. On the other hand, the detrimental effects of stress on the structural integrity and function of endothelial cells should not be neglected. Collectively, these data support the notion that chronic environmental stress is an important determinant of CVD risk. Further work is required to assess the magnitude of this risk, and to delineate the specific mechanisms by which environmental toxins affect CVD.

Specifically, the structural and physiological properties of the neurovascular barriers (i.e., blood–brain barrier (BBB), inner blood–retinal barrier (iBRB), and blood labyrinth barrier (BLB)) of the inner ear present a challenging obstacle to drug delivery to the central nervous system (CNS), limiting the treatment of many CNS diseases. The therapeutic molecule must reach the target cell in a sufficient concentration and in a suitable time frame for the treatment to be effective. Different approaches to improve drug delivery and circumvent the BBB may be local, regional, or global, and can be simulated by using in silico, in vitro, and in vivo models to understand and improve the specific mechanisms of drug permeation across the BBB. Overall, these experimental and theoretical techniques and strategies, with differing levels of complexity, could provide novel insights and future directions for improving diagnosis and treatment, as well as provide a deeper understanding of BBB-related neuropathological events.

In this Special Issue, we invite contributions that address the role of endothelial dysfunction in the development of cardiovascular and cerebrovascular diseases via extrinsic factors (environmental determinants, lifestyle, etc.) in combination with intrinsic risk factors (age-related changes), as well as contributions based on bioinformatics approaches to develop new avenues for prevention, diagnosis, and therapy.

Prof. Dr. Carola Yvette Förster
Dr. Brandon Kim
Prof. Dr. Sergey Shityakov
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. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

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

  • endothelial cells
  • endothelial dysfunction
  • angiogenesis
  • vascular endothelial cell
  • blood coagulation-fibrinolytic system
  • vascular tone
  • endothelial permeability and inflammation
  • blood-brain barrier
  • neurovascular barriers
  • tight junctions

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Published Papers (5 papers)

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Research

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22 pages, 5410 KiB  
Article
Blood Biomarkers in Takotsubo Syndrome Point to an Emerging Role for Inflammaging in Endothelial Pathophysiology
by Michiaki Nagai, Sergey Shityakov, Manuel Smetak, Hannah Jill Hunkler, Christian Bär, Nicolas Schlegel, Thomas Thum and Carola Yvette Förster
Biomolecules 2023, 13(6), 995; https://doi.org/10.3390/biom13060995 - 15 Jun 2023
Cited by 1 | Viewed by 2543
Abstract
Takotsubo syndrome (TTS), an acute cardiac condition characterized by transient wall motion abnormalities mostly of the left ventricle, results in difficulties in diagnosing patients. We set out to present a detailed blood analysis of TTS patients analyzing novel markers to understand the development [...] Read more.
Takotsubo syndrome (TTS), an acute cardiac condition characterized by transient wall motion abnormalities mostly of the left ventricle, results in difficulties in diagnosing patients. We set out to present a detailed blood analysis of TTS patients analyzing novel markers to understand the development of TTS. Significant differences in proinflammatory cytokine expression patterns and sex steroid and glucocorticoid receptor (GR) expression levels were observed in the TTS patient collected. Remarkably, the measured catecholamine serum concentrations determined from TTS patient blood could be shown to be two orders of magnitude lower than the levels determined from experimentally induced TTS in laboratory animals. Consequently, the exposure of endothelial cells and cardiomyocytes in vitro to such catecholamine concentrations did not damage the cellular integrity or function of either endothelial cells forming the blood–brain barrier, endothelial cells derived from myocardium, or cardiomyocytes in vitro. Computational analysis was able to link the identified blood markers, specifically, the proinflammatory cytokines and glucocorticoid receptor GR to microRNA (miR) relevant in the ontogeny of TTS (miR-15) and inflammation (miR-21, miR-146a), respectively. Amongst the well-described risk factors of TTS (older age, female sex), inflammaging-related pathways were identified to add to these relevant risk factors or prediagnostic markers of TTS. Full article
(This article belongs to the Special Issue Regulation of the Endothelial Cell Barrier)
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20 pages, 6474 KiB  
Article
Tumor Treating Fields (TTFields) Reversibly Permeabilize the Blood–Brain Barrier In Vitro and In Vivo
by Ellaine Salvador, Almuth F. Kessler, Dominik Domröse, Julia Hörmann, Clara Schaeffer, Aiste Giniunaite, Malgorzata Burek, Catherine Tempel-Brami, Tali Voloshin, Alexandra Volodin, Adel Zeidan, Moshe Giladi, Ralf-Ingo Ernestus, Mario Löhr, Carola Y. Förster and Carsten Hagemann
Biomolecules 2022, 12(10), 1348; https://doi.org/10.3390/biom12101348 - 22 Sep 2022
Cited by 23 | Viewed by 5756
Abstract
Despite the availability of numerous therapeutic substances that could potentially target CNS disorders, an inability of these agents to cross the restrictive blood–brain barrier (BBB) limits their clinical utility. Novel strategies to overcome the BBB are therefore needed to improve drug delivery. We [...] Read more.
Despite the availability of numerous therapeutic substances that could potentially target CNS disorders, an inability of these agents to cross the restrictive blood–brain barrier (BBB) limits their clinical utility. Novel strategies to overcome the BBB are therefore needed to improve drug delivery. We report, for the first time, how Tumor Treating Fields (TTFields), approved for glioblastoma (GBM), affect the BBB’s integrity and permeability. Here, we treated murine microvascular cerebellar endothelial cells (cerebEND) with 100–300 kHz TTFields for up to 72 h and analyzed the expression of barrier proteins by immunofluorescence staining and Western blot. In vivo, compounds normally unable to cross the BBB were traced in healthy rat brain following TTFields administration at 100 kHz. The effects were analyzed via MRI and immunohistochemical staining of tight-junction proteins. Furthermore, GBM tumor-bearing rats were treated with paclitaxel (PTX), a chemotherapeutic normally restricted by the BBB combined with TTFields at 100 kHz. The tumor volume was reduced with TTFields plus PTX, relative to either treatment alone. In vitro, we demonstrate that TTFields transiently disrupted BBB function at 100 kHz through a Rho kinase-mediated tight junction claudin-5 phosphorylation pathway. Altogether, if translated into clinical use, TTFields could represent a novel CNS drug delivery strategy. Full article
(This article belongs to the Special Issue Regulation of the Endothelial Cell Barrier)
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Review

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20 pages, 2935 KiB  
Review
Linking Cerebrovascular Dysfunction to Age-Related Hearing Loss and Alzheimer’s Disease—Are Systemic Approaches for Diagnosis and Therapy Required?
by Carola Y. Förster, Sergey Shityakov, Verena Scheper and Thomas Lenarz
Biomolecules 2022, 12(11), 1717; https://doi.org/10.3390/biom12111717 - 19 Nov 2022
Cited by 8 | Viewed by 3581
Abstract
Alzheimer’s disease (AD), the most common cause of dementia in the elderly, is a neurodegenerative disorder associated with neurovascular dysfunction, cognitive decline, and the accumulation of amyloid β peptide (Aβ) in the brain and tau-related lesions in neurons termed neurofibrillary tangles (NFTs). Aβ [...] Read more.
Alzheimer’s disease (AD), the most common cause of dementia in the elderly, is a neurodegenerative disorder associated with neurovascular dysfunction, cognitive decline, and the accumulation of amyloid β peptide (Aβ) in the brain and tau-related lesions in neurons termed neurofibrillary tangles (NFTs). Aβ deposits and NFT formation are the central pathological hallmarks in AD brains, and the majority of AD cases have been shown to exhibit a complex combination of systemic comorbidities. While AD is the foremost common cause of dementia in the elderly, age-related hearing loss (ARHL) is the most predominant sensory deficit in the elderly. During aging, chronic inflammation and resulting endothelial dysfunction have been described and might be key contributors to AD; we discuss an intriguing possible link between inner ear strial microvascular pathology and blood–brain barrier pathology and present ARHL as a potentially modifiable and treatable risk factor for AD development. We present compelling evidence that ARHL might well be seen as an important risk factor in AD development: progressive hearing impairment, leading to social isolation, and its comorbidities, such as frailty, falls, and late-onset depression, link ARHL with cognitive decline and increased risk of dementia, rendering it tempting to speculate that ARHL might be a potential common molecular and pathological trigger for AD. Additionally, one could speculate that amyloid-beta might damage the blood–labyrinth barrier as it does to the blood–brain barrier, leading to ARHL pathology. Finally, there are options for the treatment of ARHL by targeted neurotrophic factor supplementation to the cochlea to improve cognitive outcomes; they can also prevent AD development and AD-related comorbidity in the future. Full article
(This article belongs to the Special Issue Regulation of the Endothelial Cell Barrier)
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25 pages, 6171 KiB  
Review
The Protective Effects of Neurotrophins and MicroRNA in Diabetic Retinopathy, Nephropathy and Heart Failure via Regulating Endothelial Function
by Sergey Shityakov, Michiaki Nagai, Süleyman Ergün, Barbara M. Braunger and Carola Y. Förster
Biomolecules 2022, 12(8), 1113; https://doi.org/10.3390/biom12081113 - 12 Aug 2022
Cited by 12 | Viewed by 3858
Abstract
Diabetes mellitus is a common disease affecting more than 537 million adults worldwide. The microvascular complications that occur during the course of the disease are widespread and affect a variety of organ systems in the body. Diabetic retinopathy is one of the most [...] Read more.
Diabetes mellitus is a common disease affecting more than 537 million adults worldwide. The microvascular complications that occur during the course of the disease are widespread and affect a variety of organ systems in the body. Diabetic retinopathy is one of the most common long-term complications, which include, amongst others, endothelial dysfunction, and thus, alterations in the blood-retinal barrier (BRB). This particularly restrictive physiological barrier is important for maintaining the neuroretina as a privileged site in the body by controlling the inflow and outflow of fluid, nutrients, metabolic end products, ions, and proteins. In addition, people with diabetic retinopathy (DR) have been shown to be at increased risk for systemic vascular complications, including subclinical and clinical stroke, coronary heart disease, heart failure, and nephropathy. DR is, therefore, considered an independent predictor of heart failure. In the present review, the effects of diabetes on the retina, heart, and kidneys are described. In addition, a putative common microRNA signature in diabetic retinopathy, nephropathy, and heart failure is discussed, which may be used in the future as a biomarker to better monitor disease progression. Finally, the use of miRNA, targeted neurotrophin delivery, and nanoparticles as novel therapeutic strategies is highlighted. Full article
(This article belongs to the Special Issue Regulation of the Endothelial Cell Barrier)
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Other

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16 pages, 1386 KiB  
Systematic Review
The Role of Clusterin Transporter in the Pathogenesis of Alzheimer’s Disease at the Blood–Brain Barrier Interface: A Systematic Review
by Muhammad Mazhar Fareed, Maryam Qasmi, Shaan Aziz, Elisabeth Völker, Carola Yvette Förster and Sergey Shityakov
Biomolecules 2022, 12(10), 1452; https://doi.org/10.3390/biom12101452 - 10 Oct 2022
Cited by 8 | Viewed by 3325
Abstract
Alzheimer’s disease (AD) is considered a chronic and debilitating neurological illness that is increasingly impacting older-age populations. Some proteins, including clusterin (CLU or apolipoprotein J) transporter, can be linked to AD, causing oxidative stress. Therefore, its activity can affect various functions [...] Read more.
Alzheimer’s disease (AD) is considered a chronic and debilitating neurological illness that is increasingly impacting older-age populations. Some proteins, including clusterin (CLU or apolipoprotein J) transporter, can be linked to AD, causing oxidative stress. Therefore, its activity can affect various functions involving complement system inactivation, lipid transport, chaperone activity, neuronal transmission, and cellular survival pathways. This transporter is known to bind to the amyloid beta (Aβ) peptide, which is the major pathogenic factor of AD. On the other hand, this transporter is also active at the blood–brain barrier (BBB), a barrier that prevents harmful substances from entering and exiting the brain. Therefore, in this review, we discuss and emphasize the role of the CLU transporter and CLU-linked molecular mechanisms at the BBB interface in the pathogenesis of AD. Full article
(This article belongs to the Special Issue Regulation of the Endothelial Cell Barrier)
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