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Molecular Basis and Advances of Targeted Therapy for Brain Endothelial Dysfunction

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

Deadline for manuscript submissions: closed (15 February 2024) | Viewed by 6409

Special Issue Editor

Prof. Dr. Aloïse Mabondzo

E-Mail Website
Guest Editor
Neurovascular Unit Research & Therapeutic Innovation Lab (LENIT), Department of Medicines and Healthcare Technologies, The French Alternative Energies and Atomic Energy Commission, Paris-Saclay University, 91191 Gif-sur-Yvette, France
Interests: neurodegenerative diseases; rare brain disease; CNS drug delivery; brain modeling; blood–brain barrier dysfunction; blood–brain barrier target

Special Issue Information

Dear Colleagues,

The International Journal of Molecular Science is pleased to announce a new Special Issue entitled "Molecular Basis and Advances of Targeted Therapy for Brain Endothelial Dysfunction”, for which Dr. Aloïse Mabondzo is serving as the Guest Editor. The topic is of importance since neuronal-impairment-caused neurodegenerative and metabolic disease is a major contributor to physical, cognitive, and psychological disability worldwide. Treatment of brain diseases has failed to demonstrate clinical efficacy, possibly due to a focus on the neuronal compartment and disregard for blood–brain barrier (BBB) dysfunction. The search of effective and safe therapies for brain diseases needs to fulfill key tasks of understanding the specific functions of the neurovasculature and identifying the molecular attributes underlying the barrier mechanisms. These key aspects are critical not only to designing drug delivery strategies in order to reach pharmacologically significant central nervous levels, but also to identifying pharmacological targets at the BBB in order to restore or normalize its functions in degenerative, cerebral ischemia and metabolic diseases. 

We invite you to submit your paper focusing on the molecular basis of and advances in targeted therapy for brain endothelial dysfunction. Since IJMS is a journal of molecular science, pure clinical or model studies will not be suitable. However, clinical or pure model submissions with biomolecular experiments are welcomed.

Prof. Dr. Aloïse Mabondzo
Guest Editor

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • brain endothelial cells
  • blood–brain barrier dysfunction
  • therapeutic approaches
  • blood–brain barrier target in brain diseases
  • interplay between the neuronal network and the blood–brain barrier

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Published Papers (3 papers)

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Research

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18 pages, 3065 KiB  
Article
Effects of Prokineticins on Cerebral Cell Function and Blood–Brain Barrier Permeability
by Hadi Younes, Ioanna Kyritsi, Zineb Mahrougui, Mohamed Benharouga, Nadia Alfaidy and Christel Marquette
Int. J. Mol. Sci. 2023, 24(20), 15428; https://doi.org/10.3390/ijms242015428 - 21 Oct 2023
Viewed by 1614
Abstract
Prokineticins are a family of small proteins with diverse roles in various tissues, including the brain. However, their specific effects on different cerebral cell types and blood–brain barrier (BBB) function remain unclear. The aim of this study was to investigate the effects of [...] Read more.
Prokineticins are a family of small proteins with diverse roles in various tissues, including the brain. However, their specific effects on different cerebral cell types and blood–brain barrier (BBB) function remain unclear. The aim of this study was to investigate the effects of PROK1 and PROK2 on murine cerebral cell lines, bEnd.3, C8.D30, and N2a, corresponding to microvascular endothelial cells, astrocytes and neurons, respectively, and on an established BBB co-culture model. Western blot analysis showed that prokineticin receptors (PROKR1 and PROKR2) were differentially expressed in the considered cell lines. The effect of PROK1 and PROK2 on cell proliferation and migration were assessed using time-lapse microscopy. PROK1 decreased neural cells’ proliferation, while it had no effect on the proliferation of endothelial cells and astrocytes. In contrast, PROK2 reduced the proliferation of all cell lines tested. Both PROK1 and PROK2 increased the migration of all cell lines. Blocking PROKRs with the PROKR1 antagonist (PC7) and the PROKR2 antagonist (PKR-A) inhibited astrocyte PROK2-mediated migration. Using the insert co-culture model of BBB, we demonstrated that PROKs increased BBB permeability, which could be prevented by PROKRs’ antagonists. Full article
(This article belongs to the Special Issue Molecular Basis and Advances of Targeted Therapy for Brain Endothelial Dysfunction)
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15 pages, 9116 KiB  
Article
Effects of Voluntary Physical Exercise on the Neurovascular Unit in a Mouse Model of Alzheimer’s Disease
by Jesús Andrade-Guerrero, Erika Orta-Salazar, Citlaltepetl Salinas-Lara, Carlos Sánchez-Garibay, Luis Daniel Rodríguez-Hernández, Isaac Vargas-Rodríguez, Nayeli Barron-Leon, Carlos Ledesma-Alonso, Sofía Diaz-Cintra and Luis O. Soto-Rojas
Int. J. Mol. Sci. 2023, 24(13), 11134; https://doi.org/10.3390/ijms241311134 - 6 Jul 2023
Cited by 4 | Viewed by 2415
Abstract
Alzheimer’s disease (AD) is the most common neurodegenerative disorder worldwide. Histopathologically, AD presents two pathognomonic hallmarks: (1) neurofibrillary tangles, characterized by intracellular deposits of hyperphosphorylated tau protein, and (2) extracellular amyloid deposits (amyloid plaques) in the brain vasculature (cerebral amyloid angiopathy; CAA). It [...] Read more.
Alzheimer’s disease (AD) is the most common neurodegenerative disorder worldwide. Histopathologically, AD presents two pathognomonic hallmarks: (1) neurofibrillary tangles, characterized by intracellular deposits of hyperphosphorylated tau protein, and (2) extracellular amyloid deposits (amyloid plaques) in the brain vasculature (cerebral amyloid angiopathy; CAA). It has been proposed that vascular amyloid deposits could trigger neurovascular unit (NVU) dysfunction in AD. The NVU is composed primarily of astrocytic feet, endothelial cells, pericytes, and basement membrane. Although physical exercise is hypothesized to have beneficial effects against AD, it is unknown whether its positive effects extend to ameliorating CAA and improving the physiology of the NVU. We used the triple transgenic animal model for AD (3xTg-AD) at 13 months old and analyzed through behavioral and histological assays, the effect of voluntary physical exercise on cognitive functions, amyloid angiopathy, and the NVU. Our results show that 3xTg-AD mice develop vascular amyloid deposits which correlate with cognitive deficits and NVU alteration. Interestingly, the physical exercise regimen decreases amyloid angiopathy and correlates with an improvement in cognitive function as well as in the underlying integrity of the NVU components. Physical exercise could represent a key therapeutic approach in cerebral amyloid angiopathy and NVU stability in AD patients. Full article
(This article belongs to the Special Issue Molecular Basis and Advances of Targeted Therapy for Brain Endothelial Dysfunction)
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Review

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16 pages, 615 KiB  
Review
Targeting the Multiple Complex Processes of Hypoxia-Ischemia to Achieve Neuroprotection
by Auriane Maïza, Rifat Hamoudi and Aloïse Mabondzo
Int. J. Mol. Sci. 2024, 25(10), 5449; https://doi.org/10.3390/ijms25105449 - 17 May 2024
Viewed by 1847
Abstract
Hypoxic-ischemic encephalopathy (HIE) is a major cause of newborn brain damage stemming from a lack of oxygenated blood flow in the neonatal period. Twenty-five to fifty percent of asphyxiated infants who develop HIE die in the neonatal period, and about sixty percent of [...] Read more.
Hypoxic-ischemic encephalopathy (HIE) is a major cause of newborn brain damage stemming from a lack of oxygenated blood flow in the neonatal period. Twenty-five to fifty percent of asphyxiated infants who develop HIE die in the neonatal period, and about sixty percent of survivors develop long-term neurological disabilities. From the first minutes to months after the injury, a cascade of events occurs, leading to blood-brain barrier (BBB) opening, neuronal death and inflammation. To date, the only approach proposed in some cases is therapeutic hypothermia (TH). Unfortunately, TH is only partially protective and is not applicable to all neonates. This review synthesizes current knowledge on the basic molecular mechanisms of brain damage in hypoxia-ischemia (HI) and on the different therapeutic strategies in HI that have been used and explores a major limitation of unsuccessful therapeutic approaches. Full article
(This article belongs to the Special Issue Molecular Basis and Advances of Targeted Therapy for Brain Endothelial Dysfunction)
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