Dataset Information

Integration of transcriptomics, proteomics and metabolomics data to reveal the biological mechanisms of abrin injury in human lung epithelial cells

ABSTRACT: we performed a comprehensive analysis of transcriptomics, proteomics and metabolomics on the potential mechanism of abrin injury in human lung epithelial cells.

ORGANISM(S): Homo Sapiens

SUBMITTER: Wensen Liu

PROVIDER: PXD012435 | iProX | Fri Jan 18 00:00:00 GMT 2019

REPOSITORIES: iProX

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Integration of transcriptomics, proteomics and metabolomics data to reveal the biological mechanisms of abrin injury in human lung epithelial cells.

Zhu Wenhe W Yu Haotian H Wang Yan Y Chang Ying Y Wan Jiayu J Xu Na N Wang Jinglin J Liu Wensen W

Toxicology letters 20190501

<h4>Background</h4>Abrin toxin (AT) is a potent plant toxin that belongs to the type Ⅱ ribosome inactivating protein family and is recognized as an important toxin agent for potential bioweapons. Exposure to AT by way of aerosol is the most lethal route, but the mechanism of injury requires further investigation.<h4>Materials and methods</h4>In the present study, we performed a comprehensive analysis of transcriptomics, proteomics and metabolomics on the potential mechanism of abrin injury in hu ...[more]

PMID: 31054353

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Project description:Background Acute pancreatitis (AP) is a severe inflammatory disease that frequently causes multi-organ damage, with intestinal injury being a major complication. The mechanisms underlying SAP-induced intestinal injury remain unclear, particularly regarding spatial cellular reorganization and functional interactions. Methods This study constructed a severe acute pancreatitis (SAP) rat model and employed single-nucleus RNA sequencing (snRNA-seq) and spatial transcriptome sequencing (stRNA-seq) technologies to systematically analyze the dynamic changes in intestinal cellular composition, spatial distribution, and function during SAP-induced intestinal injury. Results snRNA-seq identified 18 major ileal cell populations spanning epithelial, immune, stem/TA, and stromal compartments. SAP was associated with compositional remodeling characterized by downward trends in Lgr5⁺/Olfm4⁺ stem cells, TA1, goblet cells, and Paneth cells, with a reciprocal increase in enterocytes, although most proportion changes did not reach statistical significance at the animal level. Spatial transcriptomics independently captured SAP-associated tissue remodeling, including a significant reduction in Paneth cells accompanied by increases in fat cells, macrophages, goblet cells, and TA2 cells. Across epithelial lineages, SAP induced a transcriptional shift toward immune interaction with up-regulation of antigen presentation–related genes (e.g., Cd74, Apoa1) and down-regulation of antimicrobial/barrier effectors (e.g., Defa24, Pla2g2a, Dmbt1), which was corroborated by spatial expression patterns and spatially variable gene programs enriched for host defense responses. Pseudotime analysis suggested a redistribution of epithelial states along the stem/TA-to-enterocyte continuum, with relative depletion of early states and expansion of enterocyte-dominant states in SAP. CellChat analysis revealed globally intensified intercellular communication and nominated FN1 as the pathway with the highest differential information flow, with Lgr5⁺ stem cells predicted as prominent FN1 senders targeting enterocytes and smooth muscle cells. SCENIC identified reduced activity and expression of Hmga2/Myb regulons in stem compartments, and immunofluorescence showed decreasing trends in Hmga2/Myb-positive Olfm4⁺ and Lgr5⁺ stem cells in SAP. Conclusions Integrated single-nucleus and spatial transcriptomics reveal that SAP is accompanied by spatially organized ileal remodeling, epithelial immune-interacting rewiring, and altered neighborhood architecture, together with an ECM-centered FN1 signaling axis and attenuated Hmga2/Myb-associated regulatory programs in stem compartments. These findings provide a spatially informed cellular framework and generate testable hypotheses for mechanisms underlying impaired epithelial regeneration during SAP-associated intestinal injury.

Dataset Information

Integration of transcriptomics, proteomics and metabolomics data to reveal the biological mechanisms of abrin injury in human lung epithelial cells

Publications

Integration of transcriptomics, proteomics and metabolomics data to reveal the biological mechanisms of abrin injury in human lung epithelial cells.

Similar Datasets

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