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Molecular Research and Therapeutic Targets in Acute Settings: Ischemic and Traumatic Brain Injuries

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: 30 July 2024 | Viewed by 979

Special Issue Editor


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Guest Editor
Department of Pediatrics, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY 10032, USA
Interests: cute hypoxic-ischemic injuries

Special Issue Information

Dear Colleagues,

The pathophysiology of cerebral ischemia and brain trauma indicates that similar mechanisms contribute to the loss of cellular integrity and tissue damage.

Brain injuries result from the complex interplay of multiple pathways including excitotoxicity, ionic imbalance, oxidative/nitrative stress and blood–brain barrier (BBB) disruption. With cell type-specific pathomechanisms, acute cerebral insults activate neuronal cell death, inflammation from microglia activation and immune cell infiltration, accompanied with astrogliosis, and complex glia–neuron exchanges, and they are important elements in the pathological onset and the progression of ischemic or trauma-triggered brain damage.

From exploring these molecular mechanisms and dissecting the role of specific cell-type signaling pathways or cell–cell interactions, each contribution will aim to provide insights that pave the way for more effective therapeutic approaches.

I look forward to receiving your contributions.

Dr. Hylde Zirpoli
Guest Editor

Manuscript Submission Information

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Keywords

  • ischemic brain injury
  • traumatic brain insult
  • cell-type specific molecular mechanisms
  • therapy
  • target discovery
  • repurposing
  • efficacy studies
  • new drug formulations
  • high-throughput technologies
  • proteomics
  • metabolomics
  • microarray
  • next-generation sequencing
  • BBB disruption
  • gliosis
  • neuronal loss
  • neurobehavior
  • age-related molecular mechanisms in brain injury

Published Papers (1 paper)

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Research

20 pages, 18479 KiB  
Article
Pulmonary Effects of Traumatic Brain Injury in Mice: A Gene Set Enrichment Analysis
by Wei-Hung Chan, Shih-Ming Huang and Yi-Lin Chiu
Int. J. Mol. Sci. 2024, 25(5), 3018; https://doi.org/10.3390/ijms25053018 - 05 Mar 2024
Viewed by 763
Abstract
Acute lung injury occurs in 20–25% of cases following traumatic brain injury (TBI). We investigated changes in lung transcriptome expression post-TBI using animal models and bioinformatics. Employing unilateral controlled cortical impact for TBI, we conducted microarray analysis after lung acquisition, followed by gene [...] Read more.
Acute lung injury occurs in 20–25% of cases following traumatic brain injury (TBI). We investigated changes in lung transcriptome expression post-TBI using animal models and bioinformatics. Employing unilateral controlled cortical impact for TBI, we conducted microarray analysis after lung acquisition, followed by gene set enrichment analysis of differentially expressed genes. Our findings indicate significant upregulation of inflammation-related genes and downregulation of nervous system genes. There was enhanced infiltration of adaptive immune cells, evidenced by positive enrichment in Lung-Th1, CD4, and CD8 T cells. Analysis using the Tabula Sapiens database revealed enrichment in lung-adventitial cells, pericytes, myofibroblasts, and fibroblasts, indicating potential effects on lung vasculature and fibrosis. Gene set enrichment analysis linked TBI to lung diseases, notably idiopathic pulmonary hypertension. A Venn diagram overlap analysis identified a common set of 20 genes, with FOSL2 showing the most significant fold change. Additionally, we observed a significant increase in ADRA1AIL6 production post-TBI using the L1000 library. Our study highlights the impact of brain trauma on lung injury, revealing crucial gene expression changes related to immune cell infiltration, cytokine production, and potential alterations in lung vasculature and fibrosis, along with a specific spectrum of disease influence. Full article
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