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<p>Traumatic brain injury (TBI) induces profound functional heterogeneity in astrocytes, yet the regulatory mechanisms underlying this diversity remain poorly understood. In this study, we analyzed single-cell RNA sequencing data from the cortex and hippocampus of TBI mouse models to characterize astrocyte subtypes and their functional dynamics. We identified two major reactive subtypes: A1 astrocytes, enriched in inflammatory response, synaptic regulation, and neurodegenerative disease-related pathways; and A2 astrocytes, enriched in lipid metabolism, extracellular matrix (ECM) remodeling, and phagosome formation pathways. These functional differences were consistently observed across datasets with varying injury severities. Notably, adhesion-related pathways—including gap junctions, adherens junctions, and calcium-dependent adhesion—showed significant subtype-specific expression patterns and temporal shifts. Pseudotime trajectory analysis further suggested a potential transition between A1 and A2 states, accompanied by dynamic regulation of adhesion-related genes. Our findings highlight the complex and context-dependent roles of astrocytes in TBI and propose cell adhesion as a key modulator of astrocyte functional polarization.</p>

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Adhesion-Related Pathways and Functional Polarization of Astrocytes in Traumatic Brain Injury: Insights from Single-cell RNA Sequencing

  • 期刊论文

  • 发表日期：

    2025年4月27日

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  • Xiaoyan Liu,
  • Ji Xia,
  • Wenjing Shao,
  • Xiaoming Li,
  • Danfeng Yuan,
  • Jingru Xie,
  • Liang Zhang,
  • Yuqian Tang,
  • Hui Zhao,
  • Pengfei Wu

摘要

Traumatic brain injury (TBI) induces profound functional heterogeneity in astrocytes, yet the regulatory mechanisms underlying this diversity remain poorly understood. In this study, we analyzed single-cell RNA sequencing data from the cortex and hippocampus of TBI mouse models to characterize astrocyte subtypes and their functional dynamics. We identified two major reactive subtypes: A1 astrocytes, enriched in inflammatory response, synaptic regulation, and neurodegenerative disease-related pathways; and A2 astrocytes, enriched in lipid metabolism, extracellular matrix (ECM) remodeling, and phagosome formation pathways. These functional differences were consistently observed across datasets with varying injury severities. Notably, adhesion-related pathways—including gap junctions, adherens junctions, and calcium-dependent adhesion—showed significant subtype-specific expression patterns and temporal shifts. Pseudotime trajectory analysis further suggested a potential transition between A1 and A2 states, accompanied by dynamic regulation of adhesion-related genes. Our findings highlight the complex and context-dependent roles of astrocytes in TBI and propose cell adhesion as a key modulator of astrocyte functional polarization.