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Related Experiment Video

Updated: May 28, 2025

Three-dimensional Confocal Analysis of Microglia/macrophage Markers of Polarization in Experimental Brain Injury
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Changes in border-associated macrophages after stroke: Single-cell sequencing analysis.

Ning Yu1, Yang Zhao, Peng Wang

  • 1Department of Anesthesiology, Shandong Provincial Key Medical and Health Laboratory of Anesthesia and Brain Function (The Affiliated Hospital of Qingdao University), The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China.

Neural Regeneration Research
|February 10, 2025
PubMed
Summary
This summary is machine-generated.

Border-associated macrophages play a key role in stroke-induced inflammation. Targeting these cells, particularly the signal transducer and activator of transcription 3 (Stat3) pathway, may offer a new therapeutic strategy for stroke treatment.

Keywords:
STAT3border-associated macrophagesclodronatehypoxiaischemia-reperfusionischemic strokeliposomesneuroinflammationsingle-cell sequencing analysistumor necrosis factor

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Area of Science:

  • Neuroimmunology
  • Stroke Pathophysiology
  • Single-cell Genomics

Background:

  • Border-associated macrophages (BAMs) reside at brain-periphery interfaces and their functions, especially in neuroinflammation, are under-explored.
  • Recent findings suggest BAMs involvement in stroke-induced inflammation, but underlying mechanisms require elucidation.

Purpose of the Study:

  • To comprehensively analyze the transcriptional profile and communication networks of mouse BAMs post-stroke.
  • To identify key molecular pathways and transcription factors involved in BAMs' response to ischemic stroke.
  • To evaluate the therapeutic potential of targeting BAMs in a preclinical stroke model.

Main Methods:

  • Single-cell RNA sequencing data analysis (GEO datasets GSE174574, GSE225948).
  • Differential gene expression, enrichment analysis, and CellChat analysis for cell communication.
  • Transcription factor prediction using pySCENIC.
  • Pharmacological depletion of BAMs using clodronate liposomes in a mouse stroke model.

Main Results:

  • BAMs exhibit dynamic transcriptional changes and regulate inflammatory pathways, including the tumor necrosis factor pathway, post-ischemic stroke.
  • Signal transducer and activator of transcription 3 (Stat3) activity is significantly upregulated in BAMs following stroke.
  • Depletion of BAMs using clodronate liposomes reduced infarct volume and improved neurological scores in a mouse stroke model.

Conclusions:

  • Stroke induces significant transcriptional alterations in BAMs, implicating them in neuroinflammation.
  • Stat3 signaling in BAMs represents a potential therapeutic target for mitigating stroke-induced neuroinflammation.
  • Targeting BAMs offers a promising strategy for stroke treatment, supported by preclinical evidence of reduced brain injury.