Traumatic Brain Injury in a Well: A Modular Three-Dimensional Printed Tool for Inducing Traumatic Brain Injury <i>In vitro</i>

Schlotterose, Luise; Beldjilali-Labro, Megane; Schneider, Gaya; Vardi, Ofir; Hattermann, Kirsten; Even, U.; Shohami, Esther; Haustein, Herman D.; Leichtmann-Bardoogo, Yael; Maoz, Ben M.

doi:10.1089/neur.2022.0072

Cited by 3 publications

(2 citation statements)

References 38 publications

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“…Chemical injuries are used for the microenvironment investigations of post-TBI tissues, and these include altering culture conditions with nutrient or oxygen deprivation, or treatments with chemicals [ 278 ]. Schlotterose et al [ 279 ] developed a 3D-printed device for standard and non-standard cell culture applications to induce hydrostatic pressure on cells, resulting in their perturbation. As such, they were able to provoke TBI-typical hallmarks, such as cell death, decreased neuronal functionality, neural axon swelling, and a decrease in BBB tightness.…”

Section: Disease-specific Modeling Of Neuroinflammationmentioning

confidence: 99%

Blood–Brain Barrier Breakdown in Neuroinflammation: Current In Vitro Models

Brandl,

Reindl

2023

IJMS

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The blood–brain barrier, which is formed by tightly interconnected microvascular endothelial cells, separates the brain from the peripheral circulation. Together with other central nervous system-resident cell types, including pericytes and astrocytes, the blood–brain barrier forms the neurovascular unit. Upon neuroinflammation, this barrier becomes leaky, allowing molecules and cells to enter the brain and to potentially harm the tissue of the central nervous system. Despite the significance of animal models in research, they may not always adequately reflect human pathophysiology. Therefore, human models are needed. This review will provide an overview of the blood–brain barrier in terms of both health and disease. It will describe all key elements of the in vitro models and will explore how different compositions can be utilized to effectively model a variety of neuroinflammatory conditions. Furthermore, it will explore the existing types of models that are used in basic research to study the respective pathologies thus far.

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Section: Disease-specific Modeling Of Neuroinflammationmentioning

confidence: 99%

Blood–Brain Barrier Breakdown in Neuroinflammation: Current In Vitro Models

Brandl,

Reindl

2023

IJMS

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“…These models offer the advantage of being easily controllable, widely used, and well characterized. 13 , 15–19 …”

Section: Introductionmentioning

confidence: 99%

Inducing Mechanical Stimuli to Tissues Grown on a Magnetic Gel Allows Deconvoluting the Forces Leading to Traumatic Brain Injury

Schlotterose,

Beldjilali-Labro,

Hagel

et al. 2023

Neurotrauma Reports

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Traumatic brain injury (TBI), which is characterized by damage to the brain resulting from a sudden traumatic event, is a major cause of death and disability worldwide. It has short- and long-term effects, including neuroinflammation, cognitive deficits, and depression. TBI consists of multiple steps that may sometimes have opposing effects or mechanisms, making it challenging to investigate and translate new knowledge into effective therapies. In order to better understand and address the underlying mechanisms of TBI, we have developed an in vitro platform that allows dynamic simulation of TBI conditions by applying external magnetic forces to induce acceleration and deceleration injury, which is often observed in human TBI. Endothelial and neuron-like cells were successfully grown on magnetic gels and applied to the platform. Both cell types showed an instant response to the TBI model, but the endothelial cells were able to recover quickly—in contrast to the neuron-like cells. In conclusion, the presented in vitro model mimics the mechanical processes of acceleration/deceleration injury involved in TBI and will be a valuable resource for further research on brain injury.

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Neuroprotective Role of Ranolazine: ESR1 and NMDA Receptor Agonist in Traumatic Brain Injury in Drosophila melanogaster, In Silico and In Vivo Correlation

Parvesh,

Kumar,

Singh

et al. 2024

Indian Journal of Neurotrauma

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Objective In this study, a high-impact trauma (HIT) device was used for inducing moderate traumatic brain injury (TBI) in Drosophila melanogaster. Mechanical injuries in flies caused by rapid acceleration and assertion produce symptoms characteristics of TBI in humans. Materials and Methods Docking studies were carried out to check the binding affinity of the drug toward the receptors. Various oxidative stress parameters, catalase level, glutathione level, superoxide dismutase (SOD) level, malondialdehyde (MDA), and nitric oxide levels, were measured. The mortality index and neuroprotective potential were carried out in TBI in D. melanogaster models. Results In the current study, there was an increase in oxidative stress following TBI as evidenced by a significant decrease in the catalase, glutathione, and SOD levels and increase in the level of MDA and nitric oxide after 24 hours. Antioxidant enzymes, catalase and glutathione peroxidase, have a dominant role in TBI. Docking studies were carried out on estrogen receptor 1 (pdb: 1TVO and 1UOM) and NDMA receptor (pdb: 3QEL) as agonist showing the binding affinity of the drug toward the receptors. In comparison to the vehicle-treated group, there was a dose-dependent significant increase in the SOD level and percentage climbing along with a decrease in the MDA level and total protein content. The mortality index was also observed at three concentrations of ranolazine (1, 2, and 4 mg/mL) in D. melanogaster homogenate. These findings suggest that ranolazine has a good neuroprotective potential in the treatment of TBI in the D. melanogaster model. Conclusion Present study concluded the scientific evaluation of neuroprotective potential of ranolazine in the treatment of TBI in the D. melanogaster model.

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Traumatic Brain Injury in a Well: A Modular Three-Dimensional Printed Tool for Inducing Traumatic Brain Injury In vitro

Cited by 3 publications

References 38 publications

Blood–Brain Barrier Breakdown in Neuroinflammation: Current In Vitro Models

Blood–Brain Barrier Breakdown in Neuroinflammation: Current In Vitro Models

Inducing Mechanical Stimuli to Tissues Grown on a Magnetic Gel Allows Deconvoluting the Forces Leading to Traumatic Brain Injury

Neuroprotective Role of Ranolazine: ESR1 and NMDA Receptor Agonist in Traumatic Brain Injury in Drosophila melanogaster, In Silico and In Vivo Correlation

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