bioRxiv Science⌕ Search

Biology subjects

Simbrunner, B.

Publications and source records attributed to Simbrunner, B..

2 recordsLinked to original sources

Spatial single-cell interactome and niche-specific molecular signatures in alcohol-related liver disease

Alcohol-related liver disease (ALD) remains a major global health burden with limited therapeutic options due to an incomplete understanding of its underlying molecular mechanisms and cellular crosstalk. Here, we applied ultra-high resolution (on 2 {micro}m spots) spatial transcriptomics to a cirrhotic liver tissue obtained from an end-stage ALD patient, analyzing >265,000 spatially resolved cells with further validation on single-cell and single-nuclei datasets from patients with ALD cirrhosis. Our analysis delineated distinct cellular sub-populations and molecular landscapes across fibrotic, vascular, and parenchymal niches of ALD cirrhosis. We identified robust zonation of hepatocytes, hepatic stellate cells, and diverse immune subpopulations, including enrichment of pro-inflammatory T cells and dendritic cells in the fibrotic niche and MARCO+ tissue-resident macrophages localizing mostly in parenchymal areas. Analysis of spatial metrics assigned expression of WNT4, RCAN3, PPIAL4G, PLA2G5, and SLC6A9 to the fibrotic environment in ALD. Differential expression and ligand-receptor interactome analyses revealed niche-specific signaling, with marked CCL19-CCR7 activity in fibrotic regions and DLL4-NOTCH3 crosstalk in vascular compartments. Notably, WNT4+ fibroblasts emerged as key mediators of extracellular matrix remodeling and chemoattraction, particularly via CCL19-mediated signaling towards CD8+ T cells, which was validated on single-cell resolution within the ALD cirrhotic liver in external datasets. These spatial and single-cell findings highlight novel potential therapeutic targets for patients with ALD cirrhosis.

systems biology↗

Transcriptomic signatures of progressive and regressive liver fibrosis and portal hypertension

Persistent liver injury triggers a fibrogenic program that causes pathologic remodelling of the hepatic microenvironment (i.e., liver fibrosis) and portal hypertension. The dynamics of gene regulation during liver disease progression and regression remain understudied. Here, we generated hepatic transcriptome profiles in two well-established liver disease models at peak fibrosis and during spontaneous regression after the removal of the inducing agents. We linked the dynamics of key liver disease readouts, such as portal pressure, collagen proportionate area, and transaminase serum levels, to most differentially expressed genes, enabling the identification of transcriptomic signatures of progressive vs. regressive liver fibrosis and portal hypertension. These candidate biomarkers (e.g., Scube1, Tcf4, Src, Hmga1, Trem2, Mafk, Mmp7) were also validated in RNA-seq datasets of patients with cirrhosis and portal hypertension. Finally, deconvolution analysis identified major cell types and suggested an association of macrophage and portal hepatocyte signatures with portal hypertension and fibrosis area in both models.

systems biology↗