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DOT1L enhances BLM-induced pulmonary fibrosis by inducing endothelial-to-mesenchymal transition via H3K79me2 [ChIP-seq]

ABSTRACT: Endothelial-to-mesenchymal transition (EndoMT) have been reported to contribute to pulmonary fibrosis. Here, we showed that induction of EndoMT activated DOT1L expression and enhanced H3K79me2 level by TGFβ2 in human umbilical vein endothelial cells (HUVECs) in vitro. Using a bleomycin (BLM)-induced idiopathic pulmonary fibrosis (IPF) model, endothelial-lineage tracing reporter mice, and endothelial-specific Dot1L knockout mice, we confirmed that DOT1L mediates EndoMT and drives pulmonary fibrosis in vivo through H3K79 methylation. ChIP-seq revealed direct binding of SMAD2/3 to the DOT1L promoter and increased H3K79me2 deposition at fibrosis-related genes following TGFβ2 stimulation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE297647 | GEO | 2026/04/01

REPOSITORIES: GEO

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DOT1L enhances BLM-induced pulmonary fibrosis by inducing endothelial-to-mesenchymal transition via H3K79me2 [RNA-seq]

Project description:Endothelial-to-mesenchymal transition (EndoMT) have been reported to contribute to pulmonary fibrosis. Here, we showed that induction of EndoMT activated DOT1L expression and enhanced H3K79me2 level by TGFβ2 in human umbilical vein endothelial cells (HUVECs) in vitro. Using a bleomycin (BLM)-induced idiopathic pulmonary fibrosis (IPF) model, endothelial-lineage tracing reporter mice, and endothelial-specific Dot1L knockout mice, we confirmed that DOT1L mediates EndoMT and drives pulmonary fibrosis in vivo through H3K79 methylation. ChIP-seq revealed direct binding of SMAD2/3 to the DOT1L promoter and increased H3K79me2 deposition at fibrosis-related genes following TGFβ2 stimulation.

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