ArticleAmerican journal of respiratory cell and molecular biology2012
Glucocorticoid receptor and histone deacetylase-2 mediate dexamethasone-induced repression of MUC5AC gene expression.
Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 38 citations in OpenAlex.
- Transforming Growth Factor β Inhibits MUC5AC Expression by Smad3/HDAC2 Complex Formation and NF-κB Deacetylation at K310 in NCI-H292 Cells.Molecules and cells · 2021Article
- The seven constitutive respiratory defense barriers against SARS-CoV-2 infection.Revista da Sociedade Brasileira de Medicina Tropical · 2021Review
- Chemocentric Informatics Analysis: DexamethasoneACS omega · 2020Article
- Recent Advances in the Development of Novel Drug Candidates for Regulating the Secretion of Pulmonary Mucus.Biomolecules & therapeutics · 2020Review
- Dexamethasone Treatment Increases the Intracellular Calcium Level ThroughInternational journal of molecular sciences · 2020Article
- Strategies for measuring airway mucus and mucins.Respiratory research · 2019Review
- Autocrine Acetylcholine, Induced by IL-17A via NFκB and ERK1/2 Pathway Activation, Promotes MUC5AC and IL-8 Synthesis in Bronchial Epithelial Cells.Mediators of inflammation · 2016Article
- Exploring the role and diversity of mucins in health and disease with special insight into non-communicable diseases.Glycoconjugate journal · 2015Review
- The Flavonoid 7,4'-Dihydroxyflavone Inhibits MUC5AC Gene Expression, Production, and Secretion via Regulation of NF-κB, STAT6, and HDAC2.Phytotherapy research : PTR · 2015Article
- Molecular mechanisms of repeated social defeat-induced glucocorticoid resistance: Role of microRNA.Brain, behavior, and immunity · 2015Article
- Minireview: The versatile roles of lysine deacetylases in steroid receptor signaling.Molecular endocrinology (Baltimore, Md.) · 2014Review
- IL-1β induction of MUC5AC gene expression is mediated by CREB and NF-κB and repressed by dexamethasone.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- The effect of dexamethasone on lentiviral vector infection is associated with importin αBiomedical reports · 2014Article
- Cellular and molecular biology of airway mucins.International review of cell and molecular biology · 2013Review
- Anti-inflammatory effects of budesonide in human lung fibroblast are independent of histone deacetylase 2.Journal of inflammation research · 2013Article
- CFTR, mucins, and mucus obstruction in cystic fibrosis.Cold Spring Harbor perspectives in medicine · 2012Review
- Expression of cPLAInternational journal of immunopathology and pharmacologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Airway occlusion in obstructive airway diseases is caused in part by the overproduction of secretory mucin glycoproteins through the up-regulation of mucin (MUC) genes by inflammatory mediators. Some pharmacological agents, including the glucocorticoid dexamethasone (Dex), repress mucin concentrations in lung epithelial cancer cells. Here, we show that Dex reduces the expression of MUC5AC, a major airway mucin gene, in primary differentiated normal human bronchial epithelial (NHBE) cells in a dose-dependent and time-dependent manner, and that the Dex-induced repression is mediated by the glucocorticoid receptor (GR) and two glucocorticoid response elements (GREs) in the MUC5AC promoter. The pre-exposure of cells to RU486, a GR antagonist, and mutations in either the GRE3 or GRE5 cis-sites abolished the Dex-induced repression. Chromatin immunoprecipitation (ChIP) assays showed a rapid temporal recruitment of GR to the GRE3 and GRE5 cis-elements in the MUC5AC promoter in NHBE and in A549 cells. Immunofluorescence showed nuclear colocalization of GR and histone deacetylase-2 (HDAC2) in MUC5AC-expressing NHBE cells. ChIP also showed a rapid temporal recruitment of HDAC2 to the GRE3 and GRE5 cis-elements in the MUC5AC promoter in both cell types. The knockdown of HDAC2 by HDAC2-specific short interfering RNA prevented the Dex-induced repression of MUC5AC in NHBE and A549 cells. These data demonstrate that GR and HDAC2 are recruited to the GRE3 and GRE5 cis-sites in the MUC5AC promoter and mediate the Dex-induced cis repression of MUC5AC gene expression. A better understanding of the mechanisms whereby glucocorticoids repress MUC5AC gene expression may be useful in formulating therapeutic interventions in chronic lung diseases.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.