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CUT&Tag profiling of JUND chromatin binding in human mast cell line LAD2 under SCF stimulation and imatinib perturbation

ABSTRACT: Mast cells respond to cytokine cues through rapid transcriptional rewiring. Here we generated CUT&Tag profiles of the transcription factor JUND in the human mast cell line LAD2 under three culture conditions: SCF withdrawal (EM), SCF supplementation (SCF), and SCF withdrawal plus imatinib treatment (IM). Two biological replicates were collected for each condition. Libraries were sequenced as paired-end reads and processed by adapter/quality filtering, alignment to the human reference genome (GRCh38/hg38), peak calling, and generation of normalized genome browser tracks. This dataset provides a resource to examine how SCF signaling and c-KIT pathway inhibition reshape JUND occupancy in mast cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE316333 | GEO | 2026/01/14

REPOSITORIES: GEO

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Project description:Cigarette smoke (CS)-induced airway inflammation is an important pathologic feature of chronic obstructive pulmonary disease (COPD). Recent studies suggest a potential role of JunD in the regulation of inflammation, but its role in CS-induced airway inflammation has not been reported. This study aimed to determine its role in CS-induced airway inflammation through bioinformatics analysis and in vitro and in vivo experiments. Data from the Gene Expression Omnibus (GEO) database (GSE37147) were analyzed using weighted gene co-expression network analysis (WGCNA) and key driver analysis (KDA), and these analyses were validated using the GSE47460 dataset. The effect of CS on JunD expression was examined in lung tissues of COPD patients and CS-exposed mice and in CS extract (CSE)-exposed BEAS-2B cells. The effects of CSE on airway epithelial inflammatory injury after JunD knockdown or overexpression were also investigated. mRNA-seq and chromatin immunoprecipitation (ChIP)-seq were used to explore the mechanism of JunD-mediated CS-induced airway inflammation. Mice were injected with adeno-associated virus serotype 9 (AAV9)-JunD vector or control vector and then exposed to CS for 4 weeks, and lung tissue morphology and airway inflammation were evaluated. KDA of the lung function-related gene modules in GSE37147 revealed a potential role of JunD in COPD, which was validated in GSE47460. JunD was downregulated in lung tissues of COPD patients and CS-exposed mice and in BEAS-2B cells. JunD knockdown aggravated CSE-induced tumor necrosis factor (TNF)-α and interleukin (IL)-1β release by BEAS-2B cells, while JunD overexpression attenuated these effects. mRNA-seq and ChIP-seq identified several JunD-regulated genes, which are involved in the immune response and TNF signaling pathway and are commonly dysregulated in cell models of airway inflammation. In vivo, JunD overexpression attenuated the CS-induced inflammatory cell infiltration and inflammatory cytokine release in mouse lungs. Thus, JunD is involved in CS-induced airway inflammation and JunD-based therapy may be useful in CS-induced airway disorders.

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CUT&Tag profiling of JUND chromatin binding in human mast cell line LAD2 under SCF stimulation and imatinib perturbation

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