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Related Concept Videos

Traumatic Brain Injury l: Introduction01:28

Traumatic Brain Injury l: Introduction

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DefinitionTraumatic brain injury, or TBI, is a disturbance of normal brain function induced by an external mechanical force, such as a direct blow to the head or a penetrating injury. It can affect both brain structure and function, producing a wide range of clinical outcomes. TBI is a heterogeneous condition, meaning its effects may differ based on the type, location, and severity of the injury.Basis of ClassificationTBI is classified based on severity, injury mechanism, or pathophysiology. In...
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Laser Capture Microdissection of Enriched Populations of Neurons or Single Neurons for Gene Expression Analysis After Traumatic Brain Injury
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Transcriptomic Profile of Pericontusional Tissue in Human Severe Traumatic Brain Injury.

Adaliana Sorg Mousessian Onohara1, Sueli Mieko Oba-Shinjo1, Vitor Nagai Yamaki2

  • 1Department of Neurology, Faculdade de Medicina, Laboratory of Molecular and Cellular Biology (LIM15), Universidade de Sao Paulo, Sao Paulo, SP, Brazil.

Journal of Neurotrauma
|March 11, 2026
PubMed
Summary

Traumatic brain injury (TBI) triggers inflammation and alters gene expression, affecting brain cell functions. This study identifies key signaling pathways and the CCL2-SPHK1 axis, offering potential therapeutic targets for TBI treatment.

Keywords:
humanpericontusional tissuesignaling pathwaystranscriptome analysistraumatic brain injury

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genomics

Background:

  • Traumatic brain injury (TBI) is a major cause of death and disability in young adults.
  • TBI involves complex pathophysiological events including blood-brain barrier disruption, neuronal death, and neuroinflammation.
  • Understanding TBI's molecular mechanisms is crucial for developing effective treatments.

Purpose of the Study:

  • To analyze signaling pathways in pericontusional brain tissue from severe human TBI.
  • To identify altered gene expression patterns in TBI compared to healthy controls.
  • To explore potential therapeutic targets for TBI.

Main Methods:

  • Transcriptome analysis using large-scale RNA sequencing (RNA-Seq) on human TBI brain tissue and control samples.
  • QuantSeq 3' mRNA-Seq was employed to detect differential gene expression.
  • Signaling pathway enrichment analysis and brain cell compartment analysis were performed.

Main Results:

  • Increased expression of inflammation, angiogenesis, extracellular matrix remodeling, and wound healing pathways observed in TBI.
  • Downregulation of genes related to ion transport and synaptic transmission.
  • Upregulation of pathways involving TNFα, NFkB, IL6-JAK-STAT, and others, with activation of transcription factors NFKB2, FOS, RELB, KLF4, ATF3, and EGR2.
  • Gene expression profiles indicated increased activity in microglia, immune, and endothelial cells, with decreased activity in neurons and astrocytes.
  • The CCL2-SPHK1 axis was identified and validated, linking inflammatory response to angiogenesis.

Conclusions:

  • TBI transcriptome analysis reveals differential gene expression related to inflammation and tissue repair.
  • The CCL2-SPHK1 axis plays a significant role in TBI, connecting inflammation and angiogenesis.
  • Further research into the CCL2-SPHK1 axis is warranted for its potential as a therapeutic target in TBI.