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Transient receptor potential canonical 1 channel mediates the mechanical stress ‑induced epithelial‑mesenchymal transition of human bronchial epithelial (16HBE) cells.
Transient receptor potential canonical 1 channel mediates the mechanical stress‑induced epithelial‑mesenchymal transition of human bronchial epithelial (16HBE) cells. Int J Mol Med. 2020 Apr 07;: Authors: Wang J, He Y, Yang G, Li N, Li M, Zhang M Abstract Airway remodeling is a central event in the pathology of chronic obstructive pulmonary disease (COPD) that leads to airway narrowing and subsequently, to increased mechanical pressure. High mechanical pressure can exacerbate airway remodeling. Thus, a treatment regimen aimed at disrupting this high‑pressure airway remodeling vicious cycle may i...
Source: International Journal of Molecular Medicine - April 6, 2020 Category: Molecular Biology Authors: Wang J, He Y, Yang G, Li N, Li M, Zhang M Tags: Int J Mol Med Source Type: research

Der f1 induces pyroptosis in human bronchial epithelia via the NLRP3 inflammasome.
Abstract Damage to the bronchial epithelium leads to persistent inflammation and airway remodelling in various respiratory diseases, such as asthma and chronic obstructive pulmonary disease. To date, the mechanisms underlying bronchial epithelial cell damage and death by common allergens remain largely unknown. The aim of the present study was to investigate Der f1, an allergen of Dermatophagoides farinae, which may result in the death of human bronchial epithelial cells (HBECs). Der f1 induces BECs to undergo the inflammatory cell death referred to as pyroptosis, induced by increasing lactate dehydrogenase rele...
Source: International Journal of Molecular Medicine - December 5, 2017 Category: Molecular Biology Authors: Tsai YM, Chiang KH, Hung JY, Chang WA, Lin HP, Shieh JM, Chong IW, Hsu YL Tags: Int J Mol Med Source Type: research

Caveolin-1 aggravates cigarette smoke extract-induced MUC5AC secretion in human airway epithelial cells.
In this study, we aimed to determine whether caveolin-1 modulates mucin hyperproduction induced by cigarette smoke. Our results revealed that cigarette smoke extract (CSE) significantly increased MUC5AC production, as well as the levels of phosphorylated EGFR (p-EGFR) and phosphorylated Akt (p-Akt) in human bronchial epithelial cells (16HBE cells), as shown by ELISA, RT-PCR and western blot analysis. These effects were prevented by treatment with EGFR inhibitor (AG1478) and phosphatidylinostol-3-kinase (PI3K) inhibitor (LY294002). We also found that the overexpression of caveolin-1 enhanced the expression of MUC5AC, p-EGFR...
Source: International Journal of Molecular Medicine - March 11, 2015 Category: Molecular Biology Authors: Yu Q, Chen X, Fang X, Chen Q, Hu C Tags: Int J Mol Med Source Type: research