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Keywords = cerebEND

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12 pages, 1823 KiB  
Article
Tumor Treating Fields (TTFields) Induce Cell Junction Alterations in a Human 3D In Vitro Model of the Blood-Brain Barrier
by Ellaine Salvador, Theresa Köppl, Julia Hörmann, Sebastian Schönhärl, Polina Bugaeva, Almuth F. Kessler, Malgorzata Burek, Ralf-Ingo Ernestus, Mario Löhr and Carsten Hagemann
Pharmaceutics 2023, 15(1), 185; https://doi.org/10.3390/pharmaceutics15010185 - 4 Jan 2023
Cited by 19 | Viewed by 3297
Abstract
In a recent study, we showed in an in vitro murine cerebellar microvascular endothelial cell (cerebEND) model as well as in vivo in rats that Tumor-Treating Fields (TTFields) reversibly open the blood–brain barrier (BBB). This process is facilitated by delocalizing tight junction proteins [...] Read more.
In a recent study, we showed in an in vitro murine cerebellar microvascular endothelial cell (cerebEND) model as well as in vivo in rats that Tumor-Treating Fields (TTFields) reversibly open the blood–brain barrier (BBB). This process is facilitated by delocalizing tight junction proteins such as claudin-5 from the membrane to the cytoplasm. In investigating the possibility that the same effects could be observed in human-derived cells, a 3D co-culture model of the BBB was established consisting of primary microvascular brain endothelial cells (HBMVEC) and immortalized pericytes, both of human origin. The TTFields at a frequency of 100 kHz administered for 72 h increased the permeability of our human-derived BBB model. The integrity of the BBB had already recovered 48 h post-TTFields, which is earlier than that observed in cerebEND. The data presented herein validate the previously observed effects of TTFields in murine models. Moreover, due to the fact that human cell-based in vitro models more closely resemble patient-derived entities, our findings are highly relevant for pre-clinical studies. Full article
(This article belongs to the Special Issue Targeting Cell Junctions for Therapy and Delivery)
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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 30 | Viewed by 6570
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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11 pages, 1293 KiB  
Article
Isosteviol Sodium (STVNA) Reduces Pro-Inflammatory Cytokine IL-6 and GM-CSF in an In Vitro Murine Stroke Model of the Blood–Brain Barrier (BBB)
by Moritz Reschke, Ellaine Salvador, Nicolas Schlegel, Malgorzata Burek, Srikanth Karnati, Christian Wunder and Carola Y. Förster
Pharmaceutics 2022, 14(9), 1753; https://doi.org/10.3390/pharmaceutics14091753 - 23 Aug 2022
Cited by 6 | Viewed by 2719
Abstract
Early treatment with glucocorticoids could help reduce both cytotoxic and vasogenic edema, leading to improved clinical outcome after stroke. In our previous study, isosteviol sodium (STVNA) demonstrated neuroprotective effects in an in vitro stroke model, which utilizes oxygen-glucose deprivation (OGD). Herein, we tested [...] Read more.
Early treatment with glucocorticoids could help reduce both cytotoxic and vasogenic edema, leading to improved clinical outcome after stroke. In our previous study, isosteviol sodium (STVNA) demonstrated neuroprotective effects in an in vitro stroke model, which utilizes oxygen-glucose deprivation (OGD). Herein, we tested the hypothesis that STVNA can activate glucocorticoid receptor (GR) transcriptional activity in brain microvascular endothelial cells (BMECs) as previously published for T cells. STVNA exhibited no effects on transcriptional activation of the glucocorticoid receptor, contrary to previous reports in Jurkat cells. However, similar to dexamethasone, STVNA inhibited inflammatory marker IL-6 as well as granulocyte-macrophage colony-stimulating factor (GM-CSF) secretion. Based on these results, STVNA proves to be beneficial as a possible prevention and treatment modality for brain ischemia-reperfusion injury-induced blood–brain barrier (BBB) dysfunction. Full article
(This article belongs to the Collection Women in Pharmaceutics)
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