{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Garcia-Hernandez ML"],"funding":["National Scleroderma Foundation","Rheumatology Research Foundation","Scleroderma Research Foundation"],"pagination":["e174456"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12288976"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(14)"],"pubmed_abstract":["The pathobiology of pulmonary hypertension (PH) is complex and multiple cell types contribute to disease pathogenesis. We sought to characterize the molecular crosstalk between endothelial and mesenchymal cells that promote PH in the tumor necrosis factor α-transgenic (TNF-Tg) model of PH. Pulmonary endothelial and mesenchymal cells were isolated from WT and TNF-Tg mice and underwent single-cell RNA sequencing. Data were analyzed using clustering, differential gene expression and pathway analysis, ligand-receptor interaction, transcription factor binding, and RNA velocity assessments. Significantly altered ligand-receptor interactions were confirmed with immunofluorescent staining. TNF-Tg mice had increases in smooth muscle cells and Col14+ fibroblasts, and reductions in general capillary "],"journal":["JCI insight"],"pubmed_title":["TNF drives aberrant BMP signaling to induce endothelial and mesenchymal dysregulation in pulmonary hypertension."],"pmcid":["PMC12288976"],"funding_grant_id":["n/a","R bridge award","Marta Marx Fund for the Eradication of Scleroderma"],"pubmed_authors":["Jeong Y","Rangel-Moreno J","Duemmel S","Xu Q","Bhattacharya S","Yuan K","Korman BD","Garcia-Hernandez ML","Misra R"],"additional_accession":[]},"is_claimable":false,"name":"TNF drives aberrant BMP signaling to induce endothelial and mesenchymal dysregulation in pulmonary hypertension.","description":"The pathobiology of pulmonary hypertension (PH) is complex and multiple cell types contribute to disease pathogenesis. We sought to characterize the molecular crosstalk between endothelial and mesenchymal cells that promote PH in the tumor necrosis factor α-transgenic (TNF-Tg) model of PH. Pulmonary endothelial and mesenchymal cells were isolated from WT and TNF-Tg mice and underwent single-cell RNA sequencing. Data were analyzed using clustering, differential gene expression and pathway analysis, ligand-receptor interaction, transcription factor binding, and RNA velocity assessments. Significantly altered ligand-receptor interactions were confirmed with immunofluorescent staining. TNF-Tg mice had increases in smooth muscle cells and Col14+ fibroblasts, and reductions in general capillary ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jul","modification":"2026-03-17T15:37:43.954Z","creation":"2025-08-17T03:06:15.818Z"},"accession":"S-EPMC12288976","cross_references":{"pubmed":["40569693"],"doi":["10.1172/jci.insight.174456"]}}