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Endothelial cell-derived extracellular vesicles promote sepsis-related acute lung injury by targeting and reprogramming monocytes

GSE236215 Mus musculus Expression profiling by high throughput sequencing 8 samples Submitted 2024/03/20 Platform GPL24247
Summary
Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a common life-threatening critical syndrome with no effective pharmacotherapy. Extracellular vesicles (EVs) are considered as a new way of long-distance communication between cells. Our previous research using an ex vivo perfused human ALI model suggested that endothelial cell-derived EVs (EC-EVs) mediate the development of ALI/ARDS. However, how EC-EVs aggravate lung injury remains largely unknown. Here we demonstrated that EC-EVs released under inflammatory stimulation are preferentially taken up by monocytes and reprogram the differentiation of monocytes towards M1 type macrophage. These findings demonstrate a previously unidentified mechanism by which distant infections could lead to ALI/ARDS, providing novel targets and strategies for the prevention and treatment of sepsis-related ALI/ARDS.
Published in
Endothelial cell-derived extracellular vesicles expressing surface VCAM1 promote sepsis-related acute lung injury by targeting and reprogramming monocytes
Wang L, Tang Y, Tang J et al. · Journal of extracellular vesicles 2024 · PMID 38491216 · doi:10.1002/jev2.12423
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Also filed as BioProject PRJNA989269 and SRA study SRP446665. Searching any of these in the dataset finder brings you back here.

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