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Krüppel-Like Factor 5 Regulates Airway Epithelial Cell Identity and Function [RNA-seq]

ABSTRACT: A complex network of transcription factors regulates genes involved in establishing and maintaining key biological properties of the human airway epithelium. Here we characterize the role of Krüppel-Like Factor 5 (KLF5), in controlling essential pathways of epithelial cell identity and function in the human lung. RNA-seq following siRNA-mediated depletion of KLF5 in the Calu-3 lung epithelial cell line identified significant enrichment of genes encoding chemokines and cytokines involved in the proinflammatory response, and also components of the junctional complexes mediating cell adhesion. To determine direct gene targets of KLF5, we defined the cistrome of KLF5 using ChIP-seq in both Calu-3 and 16HBE14o- lung epithelial cells lines. Occupancy site concordance analysis revealed that KLF5 co-localized with the active histone modification H3K27ac and also with binding sites for CCAAT Enhancer Binding Protein Beta (C/EBPβ). Depletion of KLF5 increased both the expression and secretion of important chemokines, a response that was enhanced following exposure to Pseudomonas aeruginosa lipopolysaccharide. Wound scratch assays in Calu-3 cells exhibited faster rates of repair after KLF5 depletion than did negative controls. Similarly, CRISPR-mediated KLF5-null 16HBE14o- cells also showed enhanced wound closure. These data reveal a pivotal role for KLF5 in coordinating epithelial functions relevant to human lung disease.

ORGANISM(S): Homo sapiens

PROVIDER: GSE164851 | GEO | 2021/10/07

REPOSITORIES: GEO

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Krüppel-Like Factor 5 Regulates Airway Epithelial Cell Identity and Function [CHIP-seq]

Project description:A complex network of transcription factors regulates genes involved in establishing and maintaining key biological properties of the human airway epithelium. Here we characterize the role of Krüppel-Like Factor 5 (KLF5), in controlling essential pathways of epithelial cell identity and function in the human lung. RNA-seq following siRNA-mediated depletion of KLF5 in the Calu-3 lung epithelial cell line identified significant enrichment of genes encoding chemokines and cytokines involved in the proinflammatory response, and also components of the junctional complexes mediating cell adhesion. To determine direct gene targets of KLF5, we defined the cistrome of KLF5 using ChIP-seq in both Calu-3 and 16HBE14o- lung epithelial cells lines. Occupancy site concordance analysis revealed that KLF5 co-localized with the active histone modification H3K27ac and also with binding sites for CCAAT Enhancer Binding Protein Beta (C/EBPβ). Depletion of KLF5 increased both the expression and secretion of important chemokines, a response that was enhanced following exposure to Pseudomonas aeruginosa lipopolysaccharide. Wound scratch assays in Calu-3 cells exhibited faster rates of repair after KLF5 depletion than did negative controls. Similarly, CRISPR-mediated KLF5-null 16HBE14o- cells also showed enhanced wound closure. These data reveal a pivotal role for KLF5 in coordinating epithelial functions relevant to human lung disease.

2021-10-07 | GSE164852 | GEO

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The Bromodomain Containing 8 (BRD8) Transcriptional Network in Human Lung Epithelial Cells [RNA-Seq]

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MiRNA expression in airway epithelial wound repair_Szczepankiewicz

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LINGO Receptor Family Members Control Epithelial Wound Healing Pathways

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2014-12-23 | E-GEOD-63397 | biostudies-arrayexpress

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