ArticleJournal of biomedicine & biotechnology2012
Triiodothyronine represses MUC5AC expression by antagonizing Sp1 binding to its promoter in human bronchial epithelial HBE16 cells.
Article in Journal of biomedicine & biotechnology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Development and Characterization of a Primary Ciliated Porcine Airway Model for the Evaluation of In Vitro Mucociliary Clearance and Mucosal Drug Delivery.Pharmaceutics · 2025Article
- Development and optimization of a differentiated airway epithelial cell model of the bovine respiratory tract.Scientific reports · 2018Article
- Optimisation of growth conditions for ovine airway epithelial cell differentiation at an air-liquid interface.PloS one · 2018Article
- Role of the type 2 iodothyronine deiodinase (D2) in the control of thyroid hormone signaling.Biochimica et biophysica acta · 2013Review
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mucus hypersecretion is a distinguished feature of chronic inflammatory airway diseases. Interestingly, in this condition thyroid function is impaired with decreased level of triiodothyronine (T3), indicating potential link between low level of T3 and mucus hypersecretion. But the underlying mechanisms are poorly understood. In this study we aimed to elucidate the effect of T3 on MUC5AC secretion in human bronchial epithelial HBE16 cells and further investigate how T3 regulates MUC5AC gene expression at transcriptional level. By RT-PCR and ELISA we showed that T3 inhibited MUC5AC mRNA expression and protein secretion in HBE16 cells. Furthermore, luciferase assay and site-directed mutagenesis analysis demonstrated that T3 repressed MUC5AC expression at transcriptional level and the mechanism might partly lie in the specific inhibition of Sp1 binding to the promoter. Our results suggest that decreased T3 level leads to the release of repression of MUC5AC expression and thus contributes to mucus hypersecretion.
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