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Controlled Cortical Impact Model for Traumatic Brain Injury
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Basp1 Intensifies Neutrophil Migration and NETs Formation in Traumatic Brain Injury.

Jianbin Sun1, Tao Li1, Tong Zhang1

  • 1Department of Biochemistry and Molecular Biology, School of Basic Medicine, Army Medical University, Chongqing, 400038, China.

Molecular Neurobiology
|May 18, 2026
PubMed
Summary

Brain abundant membrane attached signal protein 1 (Basp1) is upregulated in neutrophils after traumatic brain injury (TBI). Basp1 is crucial for neutrophil migration and neutrophil extracellular trap (NET) formation, offering a potential therapeutic target for TBI and neuroinflammation.

Keywords:
Basp1MigrationNETsNeutrophilTBI

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Area of Science:

  • Neuroscience
  • Immunology
  • Molecular Biology

Background:

  • Brain abundant membrane attached signal protein 1 (Basp1) is a neuronal growth-associated protein with poorly defined roles in peripheral diseases.
  • Recent studies suggest Basp1 modulates myeloid cell function, but its specific involvement in neuroinflammation remains unclear.
  • Neutrophils play a significant role in TBI pathogenesis, but the molecular regulators of their function in this context are not fully understood.

Purpose of the Study:

  • To investigate the role of Basp1 in neutrophil function following traumatic brain injury (TBI).
  • To elucidate the molecular mechanisms by which Basp1 influences neutrophil migration and neutrophil extracellular trap (NET) formation in TBI.
  • To evaluate Basp1 as a potential therapeutic target for TBI and other neuroinflammatory conditions.

Main Methods:

  • Re-analysis of single-cell RNA sequencing data from TBI patients.
  • Validation in a mouse TBI model using flow cytometry and tamoxifen-induced lineage tracing.
  • Bulk RNA sequencing, gene silencing, real-time PCR, protein docking, co-immunoprecipitation, and conditional knockout studies.

Main Results:

  • Basp1 was significantly upregulated in neutrophils following TBI in both human patients and a mouse model.
  • Basp1 expression in neutrophils was essential for their migration into the brain and for the formation of neutrophil extracellular traps (NETs).
  • Basp1 directly interacts with Vimentin, facilitating cytoskeletal rearrangements critical for neutrophil migration and NET formation.

Conclusions:

  • Basp1 is a key mediator of neutrophil infiltration and NET formation in the context of TBI.
  • Targeting Basp1 may represent a novel therapeutic strategy for mitigating TBI-induced neuroinflammation.
  • The findings suggest Basp1's broader potential as a therapeutic target for various neuroinflammatory diseases.