ArticleAmerican journal of respiratory cell and molecular biology2017
Glucocorticoid Receptor ChIP-Seq Identifies PLCD1 as a KLF15 Target that Represses Airway Smooth Muscle Hypertrophy.
Article in American journal of respiratory cell and molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Evolutionary Integration and Glucocorticoid Regulation of the Respiratory System: Structure, Function, and Homeostatic Adaptation.Medical sciences (Basel, Switzerland) · 2026Review
- Evaluating the Influence ofBiomolecules · 2025Article
- Enhancer RNA transcription pinpoints functional genetic variants linked to asthma.Nature communications · 2025Article
- Integrative Roles of Pro-Inflammatory Cytokines on Airway Smooth Muscle Structure and Function in Asthma.Immunological reviews · 2025Review
- Article
- Correction of transposase sequence bias in ATAC-seq data with rule ensemble modeling.NAR genomics and bioinformatics · 2023Article
- lncRNA MIR503HG Targets miR-191-5p/PLCD1 Axis and Negatively Modulates Apoptosis, Extracellular Matrix Disruption, and Inflammation in Abdominal Aortic Aneurysm.Mediators of inflammation · 2023Article
- Multiomics analysis identifies BIRC3 as a novel glucocorticoid response-associated gene.The Journal of allergy and clinical immunology · 2022Article
- Th1 cytokines synergize to change gene expression and promote corticosteroid insensitivity in pediatric airway smooth muscle.Respiratory research · 2022Article
- Intermittent glucocorticoid treatment enhances skeletal muscle performance through sexually dimorphic mechanisms.The Journal of clinical investigation · 2022Article
- Dimerization of the Glucocorticoid Receptor and Its Importance in (Patho)physiology: A Primer.Cells · 2022Review
- Insights into glucocorticoid responses derived from omics studies.Pharmacology & therapeutics · 2021Review
- Krüppel-Like Factor 15 ModulatesFrontiers in cell and developmental biology · 2021Article
- Important lessons learned from studies on the pharmacology of glucocorticoids in human airway smooth muscle cells: Too much of a good thing may be a problem.Pharmacology & therapeutics · 2020Review
- Nuclear Receptors in Asthma: Empowering Classical Molecules Against a Contemporary Ailment.Frontiers in immunology · 2020Review
- Sequencing Analysis at 8p23 Identifies Multiple Rare Variants in DLC1 Associated with Sleep-Related Oxyhemoglobin Saturation Level.American journal of human genetics · 2019Article
- Nascent transcript analysis of glucocorticoid crosstalk with TNF defines primary and cooperative inflammatory repression.Genome research · 2019Article
- Glucocorticoids and Airway Smooth Muscle: A Few More Answers, Still More Questions.American journal of respiratory cell and molecular biology · 2019Article
- Airway Smooth Muscle-Specific Transcriptomic Signatures of Glucocorticoid Exposure.American journal of respiratory cell and molecular biology · 2019Article
- Facilitating Analysis of Publicly Available ChIP-Seq Data for Integrative Studies.AMIA ... Annual Symposium proceedings. AMIA Symposium · 2019Article
Corrections and comments
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Authors and funding
6 authors.
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Abstract
Glucocorticoids exert important therapeutic effects on airway smooth muscle (ASM), yet few direct targets of glucocorticoid signaling in ASM have been definitively identified. Here, we show that the transcription factor, Krüppel-like factor 15 (KLF15), is directly induced by glucocorticoids in primary human ASM, and that KLF15 represses ASM hypertrophy. We integrated transcriptome data from KLF15 overexpression with genome-wide analysis of RNA polymerase (RNAP) II and glucocorticoid receptor (GR) occupancy to identify phospholipase C delta 1 as both a KLF15-regulated gene and a novel repressor of ASM hypertrophy. Our chromatin immunoprecipitation sequencing data also allowed us to establish numerous direct transcriptional targets of GR in ASM. Genes with inducible GR occupancy and putative antiinflammatory properties included IRS2, APPL2, RAMP1, and MFGE8. Surprisingly, we also observed GR occupancy in the absence of supplemental ligand, including robust GR binding peaks within the IL11 and LIF loci. Detection of antibody-GR complexes at these areas was abrogated by dexamethasone treatment in association with reduced RNA polymerase II occupancy, suggesting that noncanonical pathways contribute to cytokine repression by glucocorticoids in ASM. Through defining GR interactions with chromatin on a genome-wide basis in ASM, our data also provide an important resource for future studies of GR in this therapeutically relevant cell type.
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Registered trials
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