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Molecular Research of Cerebrovascular and Neurological Disorders: Role of Oxidative Stress and Pro-Inflammatory Stimuli

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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 (31 December 2020) | Viewed by 53164

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Special Issue Editors

Dr. Luca Cucullo

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Guest Editor

1. Department of Pharmaceutical Sciences, Texas Tech University Health Sciences Center, Amarillo, TX 79106, USA
2. Center for Blood Brain Barrier Research, Texas Tech University Health Sciences Center, Amarillo, TX 79106, USA
Interests: neuroscience; toxicology; in vitro modeling; biomarkers; molecular biology; redox metabolism
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Tom Abbruscato

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Guest Editor

Department of Pharmaceutical Sciences, Texas Tech University Health Sciences Center at Amarillo, Amarillo, TX 79106, USA
Interests: brain drug transport blood-brain barrier stroke neuroprotection opioid receptors smoking

Special Issue Information

Dear Colleagues,

Electrophiles and reactive oxygen species (ROS) play a major role in modulating cellular defense mechanisms as well as physiological functions and intracellular signaling. However, excessive ROS generation (endogenous and exogenous) can create a state of redox imbalance leading to concurrent inflammation and cellular/tissue damage. A growing body of research data strongly suggests that imbalanced ROS and/or electrophile overproduction are among the major prodromal factors that can impact the viability of the blood–brain barrier and promote the onset and progression of several cerebrovascular and neurodegenerative disorders. Thus, the scope of this Special Issue is to cover the molecular and mechanistic basis for the impact of ROS as well as other pro-inflammatory stimuli (either endogenous or exogenous) on the development and progression of blood–brain barrier impairment, cerebrovascular disorders, and brain damage. In addition, studies set to uncover gender susceptibility to ROS and pro-inflammatory-dependent damage as well as potential countermeasures to mitigate or neutralize the harmful effects of these pathogenic stimuli are also of great interest.

Prof. Dr. Luca Cucullo
Prof. Tom Abbruscato
Guest Editors

Manuscript Submission Information

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Keywords

blood–brain barrier
oxidative stress
inflammation
Nrf2
countermeasure
brain disorders
gender

Published Papers (4 papers)

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Research

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17 pages, 5566 KiB

Open AccessArticle

CdSe/ZnS Core-Shell-Type Quantum Dot Nanoparticles Disrupt the Cellular Homeostasis in Cellular Blood–Brain Barrier Models

by Katarzyna Dominika Kania, Waldemar Wagner and Łukasz Pułaski

Int. J. Mol. Sci. 2021, 22(3), 1068; https://doi.org/10.3390/ijms22031068 - 22 Jan 2021

Cited by 11 | Viewed by 2413

Abstract

Two immortalized brain microvascular endothelial cell lines (hCMEC/D3 and RBE4, of human and rat origin, respectively) were applied as an in vitro model of cellular elements of the blood–brain barrier in a nanotoxicological study. We evaluated the impact of CdSe/ZnS core-shell-type quantum dot nanoparticles on cellular homeostasis, using gold nanoparticles as a largely bioorthogonal control. While the investigated nanoparticles had surprisingly negligible acute cytotoxicity in the evaluated models, a multi-faceted study of barrier-related phenotypes and cell condition revealed a complex pattern of homeostasis disruption. Interestingly, some features of the paracellular barrier phenotype (transendothelial electrical resistance, tight junction protein gene expression) were improved by exposure to nanoparticles in a potential hormetic mechanism. However, mitochondrial potential and antioxidant defences largely collapsed under these conditions, paralleled by a strong pro-apoptotic shift in a significant proportion of cells (evidenced by apoptotic protein gene expression, chromosomal DNA fragmentation, and membrane phosphatidylserine exposure). Taken together, our results suggest a reactive oxygen species-mediated cellular mechanism of blood–brain barrier damage by quantum dots, which may be toxicologically significant in the face of increasing human exposure to this type of nanoparticles, both intended (in medical applications) and more often unintended (from consumer goods-derived environmental pollution). Full article

(This article belongs to the Special Issue Molecular Research of Cerebrovascular and Neurological Disorders: Role of Oxidative Stress and Pro-Inflammatory Stimuli)

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Review

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24 pages, 2432 KiB

Open AccessReview

Ambient Air Pollution Increases the Risk of Cerebrovascular and Neuropsychiatric Disorders through Induction of Inflammation and Oxidative Stress

by Omar Hahad, Jos Lelieveld, Frank Birklein, Klaus Lieb, Andreas Daiber and Thomas Münzel

Int. J. Mol. Sci. 2020, 21(12), 4306; https://doi.org/10.3390/ijms21124306 - 17 Jun 2020

Cited by 196 | Viewed by 21424

Abstract

Exposure to ambient air pollution is a well-established determinant of health and disease. The Lancet Commission on pollution and health concludes that air pollution is the leading environmental cause of global disease and premature death. Indeed, there is a growing body of evidence that links air pollution not only to adverse cardiorespiratory effects but also to increased risk of cerebrovascular and neuropsychiatric disorders. Despite being a relatively new area of investigation, overall, there is mounting recent evidence showing that exposure to multiple air pollutants, in particular to fine particles, may affect the central nervous system (CNS) and brain health, thereby contributing to increased risk of stroke, dementia, Parkinson’s disease, cognitive dysfunction, neurodevelopmental disorders, depression and other related conditions. The underlying molecular mechanisms of susceptibility and disease remain largely elusive. However, emerging evidence suggests inflammation and oxidative stress to be crucial factors in the pathogenesis of air pollution-induced disorders, driven by the enhanced production of proinflammatory mediators and reactive oxygen species in response to exposure to various air pollutants. From a public health perspective, mitigation measures are urgent to reduce the burden of disease and premature mortality from ambient air pollution. Full article

(This article belongs to the Special Issue Molecular Research of Cerebrovascular and Neurological Disorders: Role of Oxidative Stress and Pro-Inflammatory Stimuli)

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Graphical abstract

18 pages, 2124 KiB

Open AccessReview

Cerebrovascular and Neurological Dysfunction under the Threat of COVID-19: Is There a Comorbid Role for Smoking and Vaping?

by Sabrina Rahman Archie and Luca Cucullo

Int. J. Mol. Sci. 2020, 21(11), 3916; https://doi.org/10.3390/ijms21113916 - 30 May 2020

Cited by 23 | Viewed by 14092

Abstract

The recently discovered novel coronavirus, SARS-CoV-2 (COVID-19 virus), has brought the whole world to standstill with critical challenges, affecting both health and economic sectors worldwide. Although initially, this pandemic was associated with causing severe pulmonary and respiratory disorders, recent case studies reported the association of cerebrovascular-neurological dysfunction in COVID-19 patients, which is also life-threatening. Several SARS-CoV-2 positive case studies have been reported where there are mild or no symptoms of this virus. However, a selection of patients are suffering from large artery ischemic strokes. Although the pathophysiology of the SARS-CoV-2 virus affecting the cerebrovascular system has not been elucidated yet, researchers have identified several pathogenic mechanisms, including a role for the ACE2 receptor. Therefore, it is extremely crucial to identify the risk factors related to the progression and adverse outcome of cerebrovascular-neurological dysfunction in COVID-19 patients. Since many articles have reported the effect of smoking (tobacco and cannabis) and vaping in cerebrovascular and neurological systems, and considering that smokers are more prone to viral and bacterial infection compared to non-smokers, it is high time to explore the probable correlation of smoking in COVID-19 patients. Herein, we have reviewed the possible role of smoking and vaping on cerebrovascular and neurological dysfunction in COVID-19 patients, along with potential pathogenic mechanisms associated with it. Full article

(This article belongs to the Special Issue Molecular Research of Cerebrovascular and Neurological Disorders: Role of Oxidative Stress and Pro-Inflammatory Stimuli)

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21 pages, 1977 KiB

Open AccessReview

Traumatic Brain Injury and Blood–Brain Barrier (BBB): Underlying Pathophysiological Mechanisms and the Influence of Cigarette Smoking as a Premorbid Condition

by Farzane Sivandzade, Faleh Alqahtani and Luca Cucullo

Int. J. Mol. Sci. 2020, 21(8), 2721; https://doi.org/10.3390/ijms21082721 - 14 Apr 2020

Cited by 53 | Viewed by 14659

Abstract

Traumatic brain injury (TBI) is among the most pressing global health issues and prevalent causes of cerebrovascular and neurological disorders all over the world. In addition to the brain injury, TBI may also alter the systemic immune response. Thus, TBI patients become vulnerable to infections, have worse neurological outcomes, and exhibit a higher rate of mortality and morbidity. It is well established that brain injury leads to impairments of the blood–brain barrier (BBB) integrity and function, contributing to the loss of neural tissue and affecting the response to neuroprotective drugs. Thus, stabilization/protection of the BBB after TBI could be a promising strategy to limit neuronal inflammation, secondary brain damage, and acute neurodegeneration. Herein, we present a review highlighting the significant post-traumatic effects of TBI on the cerebrovascular system. These include the loss of BBB integrity and selective permeability, impact on BBB transport mechanisms, post-traumatic cerebral edema formation, and significant pathophysiological factors that may further exacerbate post-traumatic BBB dysfunctions. Furthermore, we discuss the post-traumatic impacts of chronic smoking, which has been recently shown to act as a premorbid condition that impairs post-TBI recovery. Indeed, understanding the underlying molecular mechanisms associated with TBI damage is essential to better understand the pathogenesis and progression of post-traumatic secondary brain injury and the development of targeted treatments to improve outcomes and speed up the recovery process. Therapies aimed at restoring/protecting the BBB may reduce the post-traumatic burden of TBI by minimizing the impairment of brain homeostasis and help to restore an optimal microenvironment to support neuronal repair. Full article

(This article belongs to the Special Issue Molecular Research of Cerebrovascular and Neurological Disorders: Role of Oxidative Stress and Pro-Inflammatory Stimuli)

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