Endothelial TDP-43 depletion disrupts core blood-brain barrier pathways in neurodegeneration.

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Tác giả: Ashok Cheemala, Bing Hao, Evan R Jellison, Amy L Kimble, Yunfeng Li, Patrick A Murphy, Omar M F Omar, Swati Pandey, Bo Reese, Jordan D Tyburski, Qian Wu, Riqiang Yan

Ngôn ngữ: eng

Ký hiệu phân loại: 978.02 1800–1899

Thông tin xuất bản: United States : Nature neuroscience , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 712244

Endothelial cells (ECs) help maintain the blood-brain barrier but deteriorate in many neurodegenerative disorders. Here we show, using a specialized method to isolate EC and microglial nuclei from postmortem human cortex (92 donors, 50 male and 42 female, aged 20-98 years), that intranuclear cellular indexing of transcriptomes and epitopes enables simultaneous profiling of nuclear proteins and RNA transcripts at a single-nucleus resolution. We identify a disease-associated subset of capillary ECs in Alzheimer's disease, amyotrophic lateral sclerosis and frontotemporal degeneration. These capillaries exhibit reduced nuclear β-catenin and β-catenin-downstream genes, along with elevated TNF/NF-κB markers. Notably, these transcriptional changes correlate with the loss of nuclear TDP-43, an RNA-binding protein also depleted in neuronal nuclei. TDP-43 disruption in human and mouse ECs replicates these alterations, suggesting that TDP-43 deficiency in ECs is an important factor contributing to blood-brain barrier breakdown in neurodegenerative diseases.
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