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Cells
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Identifying Molecular or Cellular Level Pathomechanisms for Possible Therapeutic/Neuroprotective Interventions...
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Identifying Molecular or Cellular Level Pathomechanisms for Possible Therapeutic/Neuroprotective Interventions in Traumatic Brain Injury

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 20 December 2024 | Viewed by 2461

Special Issue Editors

Dr. Krisztina Amrein

E-Mail Website
Guest Editor
1. Szentágothai Research Center, University of Pecs, 7624 Pecs, Hungary
2. Department of Neurosurgery, Medical School, University of Pecs, 7623 Pecs, Hungary
Interests: traumatic brain injury (head injury): biomarkers; animal models; repetitive mild TBI; coagulopathy
Dr. Endre Czeiter

E-Mail Website
Guest Editor
1. Department of Neurosurgery, Medical School, University of Pecs, H-7623 Pecs, Hungary
2. Neurotrauma Research Group, Szentagothai Research Centre, University of Pecs, H-7624 Pecs, Hungary
3. ELKH-PTE Clinical Neuroscience MR Research Group, H-7623 Pecs, Hungary
Interests: traumatic brain injury (head injury); biomarkers; animal models; histopathological consequences; repetitive mild TBI; therapeutic (neuroprotective) interventions
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is well known that traumatic brain injury represents a common clinical condition with a huge socio-economic burden. While, according to the data recently published by the Global Burden of Disease Study collaborators, there are more than 27 million new TBI cases estimated yearly worldwide associated with more than 8 million years of life lived with disability, other studies presume almost 70 thousand lethal cases in the USA and 75 thousand deaths, on top of about one million hospitalizations in Europe yearly, and all these numbers are still increasing.

Although the above-described data confirm the clear clinical need for causal (cellular level/neuroprotective) and, preferably, individualized therapeutic interventions—mainly due to the hypercomplex nature of possible pathological/pathophysiological sequelae induced by the head injury—so far (despite some clinical trials with controversial results with hypothermia, cyclosporine A and some steroid hormone analogues), there have been no real breakthroughs in this important field.

In light of the above, our current Special Issue is open to any clinical or experimental data related to any kind of promising neuroprotective interventions and/or revealed pathological alterations or pathophysiological processes which could serve as potential therapeutic targets in the near future.

Dr. Krisztina Amrein
Dr. Endre Czeiter
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. Cells is an international peer-reviewed open access semimonthly 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

  • traumatic brain injury
  • head injury
  • clinical study
  • experimental model
  • neuroprotective intervention
  • therapy
  • pathomechanism
  • molecular
  • cellular

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Published Papers (2 papers)

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26 pages, 8072 KiB  
Article
The Immune Response in Two Models of Traumatic Injury of the Immature Brain
by Zahra F. Al-Khateeb, Siân M. Henson, Jordi L. Tremoleda and Adina T. Michael-Titus
Cells 2024, 13(19), 1612; https://doi.org/10.3390/cells13191612 - 26 Sep 2024
Abstract
Traumatic brain injury (TBI) can cause major disability and increases the risk of neurodegeneration. Post-TBI, there is infiltration of peripheral myeloid and lymphoid cells; there is limited information on the peripheral immune response post-TBI in the immature brain—where injury may interfere with neurodevelopment. [...] Read more.
Traumatic brain injury (TBI) can cause major disability and increases the risk of neurodegeneration. Post-TBI, there is infiltration of peripheral myeloid and lymphoid cells; there is limited information on the peripheral immune response post-TBI in the immature brain—where injury may interfere with neurodevelopment. We carried out two injury types in juvenile mice: invasive TBI with a controlled cortical impact (CCI) and repetitive mild TBI (rmTBI) using weight drop injury and analysed the response at 5- and 35-days post-injury. In the two models, we detected the brain infiltration of immune cells (e.g., neutrophils, monocytes, dendritic cells, CD4+ T cells, and NK cells). There were increases in macrophages, neutrophils, and dendritic cells in the spleen, increases in dendritic cells in blood, and increases in CD8+ T cells and B cells in lymph nodes. These results indicate a complex peripheral immune response post-TBI in the immature brain, with differences between an invasive injury and a repetitive mild injury. Full article
(This article belongs to the Special Issue Identifying Molecular or Cellular Level Pathomechanisms for Possible Therapeutic/Neuroprotective Interventions in Traumatic Brain Injury)
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22 pages, 5825 KiB  
Article
Valproic Acid Treatment after Traumatic Brain Injury in Mice Alleviates Neuronal Death and Inflammation in Association with Increased Plasma Lysophosphatidylcholines
by Regina Hummel, Erika Dorochow, Sonja Zander, Katharina Ritter, Lisa Hahnefeld, Robert Gurke, Irmgard Tegeder and Michael K. E. Schäfer
Cells 2024, 13(9), 734; https://doi.org/10.3390/cells13090734 - 23 Apr 2024
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Abstract
The histone deacetylase inhibitor (HDACi) valproic acid (VPA) has neuroprotective and anti-inflammatory effects in experimental traumatic brain injury (TBI), which have been partially attributed to the epigenetic disinhibition of the transcription repressor RE1-Silencing Transcription Factor/Neuron-Restrictive Silencer Factor (REST/NRSF). Additionally, VPA changes post-traumatic brain [...] Read more.
The histone deacetylase inhibitor (HDACi) valproic acid (VPA) has neuroprotective and anti-inflammatory effects in experimental traumatic brain injury (TBI), which have been partially attributed to the epigenetic disinhibition of the transcription repressor RE1-Silencing Transcription Factor/Neuron-Restrictive Silencer Factor (REST/NRSF). Additionally, VPA changes post-traumatic brain injury (TBI) brain metabolism to create a neuroprotective environment. To address the interconnection of neuroprotection, metabolism, inflammation and REST/NRSF after TBI, we subjected C57BL/6N mice to experimental TBI and intraperitoneal VPA administration or vehicle solution at 15 min, 1, 2, and 3 days post-injury (dpi). At 7 dpi, TBI-induced an up-regulation of REST/NRSF gene expression and HDACi function of VPA on histone H3 acetylation were confirmed. Neurological deficits, brain lesion size, blood–brain barrier permeability, or astrogliosis were not affected, and REST/NRSF target genes were only marginally influenced by VPA. However, VPA attenuated structural damage in the hippocampus, microgliosis and expression of the pro-inflammatory marker genes. Analyses of plasma lipidomic and polar metabolomic patterns revealed that VPA treatment increased lysophosphatidylcholines (LPCs), which were inversely associated with interleukin 1 beta (Il1b) and tumor necrosis factor (Tnf) gene expression in the brain. The results show that VPA has mild neuroprotective and anti-inflammatory effects likely originating from favorable systemic metabolic changes resulting in increased plasma LPCs that are known to be actively taken up by the brain and function as carriers for neuroprotective polyunsaturated fatty acids. Full article
(This article belongs to the Special Issue Identifying Molecular or Cellular Level Pathomechanisms for Possible Therapeutic/Neuroprotective Interventions in Traumatic Brain Injury)
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