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Biology subjects

Hendrikx, T.

Publications and source records attributed to Hendrikx, T..

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↗

MicroRNA-26b protects against MASH development and can be efficiently targeted with lipid nanoparticles.

Background & AimsThe prevalence of metabolic dysfunction-associated steatohepatitis (MASH) is increasing, urging more research into the underlying mechanisms. MicroRNA-26b (miR-26b) might play a role in several MASH-related pathways. Therefore, we aimed to determine the role of miR-26b in MASH and its therapeutic potential using miR-26b mimic-loaded lipid nanoparticles (LNPs). MethodsApoe-/-Mir26b-/-, Apoe-/-LysMcreMir26bfl/fl mice, and respective controls were fed a western-type diet to induce MASH. Plasma and liver samples were characterized regarding lipid metabolism, hepatic inflammation, and fibrosis. Additionally, miR-26b mimic-loaded LNPs were injected in Apoe-/-Mir26b-/- mice to rescue the phenotype and key results were validated in human precision-cut liver slices. Finally, kinase profiling was used to elucidate underlying mechanisms. ResultsApoe-/-Mir26b-/- mice showed increased hepatic lipid levels, coinciding with increased expression of scavenger receptor a and platelet glycoprotein 4. Similar effects were found in mice lacking myeloid-specific miR-26b. Additionally, hepatic TNF and IL-6 levels and amount of infiltrated macrophages were increased in Apoe-/- Mir26b-/- mice. Moreover, Tgfb expression was increased by the miR-26b deficiency, leading to more hepatic fibrosis. A murine treatment model with miR-26b mimic-loaded LNPs reduced hepatic lipids, rescuing the observed phenotype. Kinase profiling identified increased inflammatory signaling upon miR-26b deficiency, which was rescued by LNP treatment. Finally, miR-26b mimic-loaded LNPs also reduced inflammation in human precision-cut liver slices. ConclusionsOverall, our study demonstrates that the detrimental effects of miR-26b deficiency in MASH can be rescued by LNP treatment. This novel discovery leads to more insight into MASH development, opening doors to potential new treatment options using LNP technology. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=100 SRC="FIGDIR/small/580792v2_ufig1.gif" ALT="Figure 1"> View larger version (21K): org.highwire.dtl.DTLVardef@b8b5b8org.highwire.dtl.DTLVardef@a26333org.highwire.dtl.DTLVardef@11ed2a0org.highwire.dtl.DTLVardef@963208_HPS_FORMAT_FIGEXP M_FIG C_FIG

pathology↗