空间转录组学揭示了与多发性硬化症病变一致的铜酮模型中大脑区域之间的异质性细胞-细胞相互作用。

IF 3.6 Q2 MATHEMATICAL & COMPUTATIONAL BIOLOGY
Frontiers in bioinformatics Pub Date : 2026-08-06 eCollection Date: 2026-01-01 DOI:10.3389/fbinf.2026.1832826
Hui-Hsin Tsai, Sarbottam Piya, Jing Wang, Jing Zhu, Wenxing Hu, Andrew R Gehrke, Shaolong Cao, Amanda J Guise, Su Jing Chan, Mark Sheehan, Jenhwa Chu, Zhengyu Ouyang, Matthew Ryals, Michelle Lee, Wanli Wang, Edward Zhao, Patrick Cullen, Ravi Challa, Eric Marshall, Wanyong Zeng, Yea Jin Kaeser-Woo, Chris Ehrenfels, Luke Jandreski, Helen McLaughlin, Thomas M Carlile, Jake Gagnon, Taylor L Reynolds, Mingyao Li, Kejie Li, Baohong Zhang
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引用次数: 0

摘要

cuprizone (CPZ)模型被广泛用于模拟多发性硬化症(MS)的脱髓鞘和测试潜在的髓鞘再生疗法。为了更好地理解CPZ模型的潜在病理学并评估其可翻译性,我们整合了单细胞和空间转录组学(ST)来研究大脑多个区域脱髓鞘和再鞘鞘过程中的空间细胞和分子相互作用。ST显示胼胝体(CC)以外的大脑整体脱髓鞘和神经炎症,具有区域特异性差异。我们确定少突胶质细胞和小胶质细胞是两种主要的细胞类型,在模型中具有显著的转录组变化。通过st将cpz相关的少突胶质细胞亚群(标记基因Arap2、Dock10、Tenm4、Pex5l和Dock1)和小胶质细胞亚群(标记基因ApoE、Axl、Cd9和Lpl)定位到CC。在髓鞘再生过程中,成熟的少突胶质细胞(MOL)几乎将其表型逆转回对照状态,而小胶质细胞仍与脱髓鞘表型相关。配体受体(LR)配对分析预测脱髓鞘过程中生长因子和吞噬通路的富集,这与MS病变的变化一致,并且预测小胶质细胞是主要的传递细胞。LR配对还预测了少突胶质细胞和小胶质细胞之间的高可能性相互作用,以及MOL和少突胶质细胞前体细胞(OPC)之间的新相互作用,强调了它们在去髓鞘和再髓鞘形成过程中的作用。最后,CPZ模型中的星形胶质细胞在MS病变中具有最大的疾病相关模块保存,而MOL, OPC和小胶质细胞则表现出中等至低的保存,这总体上表明CPZ模型对慢性活动性MS病变具有中等的可翻译性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Spatial transcriptomics reveal heterogeneous cell‒cell interactions among brain regions in cuprizone model consistent with multiple sclerosis lesions.

The cuprizone (CPZ) model is widely used for modeling demyelination in multiple sclerosis (MS) and for testing potential remyelination therapies. To better understand the underlying pathology of the CPZ model and evaluate its translatability, we integrated single-cell and spatial transcriptomics (ST) to investigate spatial cellular and molecular interactions during de- and remyelination in multiple brain regions. ST revealed global demyelination and neuroinflammation in the brain beyond the corpus callosum (CC), with region-specific differences. We identified oligodendroglia and microglia as two major cell types with significant transcriptomic changes in the model. CPZ-associated subclusters of oligodendroglia (marker genes Arap2, Dock10, Tenm4, Pex5l and Dock1) and microglia (marker genes ApoE, Axl, Cd9 and Lpl) were mapped to the CC by ST. During remyelination, while mature oligodendrocytes (MOL) nearly reversed their phenotype back to the control state, microglia remained associated with the demyelination phenotype. Ligand‒receptor (LR) pairing analyses predicted growth factor and phagocytic pathway enrichment during demyelination, which is consistent with changes in MS lesions, and microglia were predicted to be the major sender cells. LR pairing also predicted a high likelihood of interaction between oligodendroglia and microglia, and a novel interaction between MOL and oligodendrocyte precursor cells (OPC), underscoring their roles during de- and remyelination. Finally, astrocytes in the CPZ model had the greatest preservation of disease-associated modules in MS lesions, while MOL, OPC, and microglia showed moderate to low preservation, which overall suggests that the CPZ model has moderate translatability to chronically active MS lesions.

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