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Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

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Related Experiment Video

Updated: Jun 28, 2026

Stretch in Brain Microvascular Endothelial Cells cEND as an In Vitro Traumatic Brain Injury Model of the Blood Brain Barrier
07:19

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Traumatic Brain Injury Induces Senescence in Brain Microvasculature.

Tejal Shreeya1,2, Zsófia R Hernádi1, Zsolt K Bali3,4

  • 1Institute of Biophysics, HUN-REN Biological Research Centre, H-6726 Szeged, Hungary.

Biomolecules
|March 28, 2026
PubMed
Summary
This summary is machine-generated.

Traumatic brain injury (TBI) causes cell senescence in specific brain cells, like astrocytes and microglia, with timing varying by injury severity. This suggests cell-type specific therapies may help mitigate TBI's long-term effects.

Keywords:
NVUTBIcellular senescenceneurovascular unittraumatic brain injuryγH2AX

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathology

Background:

  • Traumatic brain injury (TBI) often results in lasting neurological impairments.
  • Cellular senescence, a state of irreversible cell cycle arrest, is increasingly linked to TBI-induced neuroinflammation and cognitive deficits.
  • The neurovascular unit (NVU) comprises glial and vascular cells crucial for brain function and integrity.

Purpose of the Study:

  • To investigate the cell-type specific patterns of cellular senescence within the NVU after experimental TBI.
  • To determine if senescence varies in glial cells (astrocytes, microglia) and vascular cells (endothelial cells, pericytes) post-TBI.
  • To explore the temporal dynamics of TBI-induced senescence in different NVU cell populations.

Main Methods:

  • Rats were subjected to single severe TBI (sTBI), single mild TBI (mTBI), or repetitive mild TBI (rmTBI).
  • Brain tissues were analyzed at 24 hours and 4 weeks post-injury using co-staining for γH2AX (a DNA damage marker) and cell type-specific markers.
  • Immunofluorescence microscopy quantified senescence in astrocytes, microglia, endothelial cells, and pericytes within the NVU.

Main Results:

  • Astrocyte senescence increased acutely following sTBI.
  • Microglial senescence was elevated in both mTBI and sTBI groups.
  • Endothelial cell senescence significantly increased in the sTBI group at the 4-week time point; pericytes showed no significant senescence.
  • Senescence was observed in specific NVU cell types, with temporal differences based on injury severity.

Conclusions:

  • TBI induces cell-type specific senescence within the NVU, with varying temporal profiles.
  • The findings highlight that glial and vascular cells exhibit differential susceptibility to TBI-induced senescence.
  • Understanding cell-specific senescence post-TBI is critical for developing targeted therapeutic strategies to manage long-term neurological consequences.