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Hydrostatic pressure driven vascular degeneration in cirrhosis [pLSEC WT/KO]

GSE244642 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2025/12/04 Platform GPL24247
Summary
The role of pathological vascular degeneration in cirrhosis remains poorly understood. In this study, we engineered multidimensional vascular models to replicate the pathological characteristics of liver sinusoidal endothelial cells (LSECs) at various fibrosis stages. Our investigation revealed that LSEC response to hydrostatic pressure is matrix stiffness-dependent, with LSECs survival when cultured on soft matrices, while those cultured on hard matrices experiencing cellular damage. The biomimic vascular in vitro model enabled us to identify GPR116 as a crucial membrane receptor of LSECs to sense and respond to hydrostatic pressure. GPR116 is specifically expressed in liver endothelial cells, and silencing GPR116 effectively protected the endothelial cells from hydrostatic pressure-induced damage on hard matrix, consequently inhibiting hepatic stellate cell activation and collagen remodeling. Thus, our findings highlight GPR116 as an indispensable pressure sensor in hepatic sinusoidal endothelium, playing a pivotal role in vascular remodeling during cirrhosis.
Published in
Hepatic hypertension on-a-chip identifies GPR116 as a hydrostatic pressure mechanosensor to regulate vascular injury in cirrhosis
Long Y, Liang K, Niu Y et al. · Science advances 2025 · PMID 41237250 · doi:10.1126/sciadv.adu7596
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Also filed as BioProject PRJNA1023951 and SRA study SRP464522. Searching any of these in the dataset finder brings you back here.

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