Endoplasmic Reticulum Stress Induces MUC5AC and MUC5B Expression in Human Nasal Airway Epithelial Cells

Kim, Y.-D.; Choi, Yoon Seok; Na, H.G.; Bae, Chang Hoon; Song, Su Jung; Kwak, Seong Yeob

doi:10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2147

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“…In particular, emerging evidence suggest that ER stress can contribute to the development and aggravation of the CRS and allergic rhinitis [ 18 , 19 ]. Moreover, we have previously reported that ER stress induces an epithelial-to-mesenchymal transition in A549 and primary nasal epithelial cells, which in turn contributes to tissue remodeling and disease recalcitrance in CRS [ 20 ]. Thus, we hypothesized ER stress to be the principle cause of chronic upper airway inflammatory disease and clearly demonstrated the underlying mechanism in nasal fibroblasts and nasal inferior turbinate tissues.…”

Section: Discussionmentioning

confidence: 99%

“…In a previous study, we found that inhibition of ER-stress through 4-PBA in airway epithelial cells suppresses epithelial-to-mesenchymal transition (EMT) of airway epithelial cells. Kim et al reported that ER-stress induces MUC5AC and MUC5B expression in human nasal airway epithelial cells and 4-PBA inhibited increased MUC5AC and MUC5B [ 20 ]. Muc5AC and MUC5B are types of mucin, and an increase in mucin in the upper airway is associated with upper airway inflammatory diseases such as allergic rhinitis and chronic rhinosinusitis.…”

Section: Discussionmentioning

confidence: 99%

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TGF-β1 Activates Nasal Fibroblasts through the Induction of Endoplasmic Reticulum Stress

et al. 2020

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(1) Background: Tissue remodeling and extracellular matrix (ECM) accumulation contribute to the development of chronic inflammatory diseases of the upper airway. Endoplasmic reticulum (ER) stress is considered to be the key signal for triggering tissue remodeling in pathological conditions. The present study aimed to investigate the role of ER-stress in TGF-β1-stimulated nasal fibroblasts and inferior turbinate organ cultures; (2) Methods: Fibroblasts and organ cultures were pretreated with 4-phenylbutyric acid (PBA) and stimulated with TGF-β1 or thapsigargin (TG). Expression of ER-stress markers, myofibroblast marker, and ECM components was measured by Western blotting and real-time PCR. Reactive oxygen species (ROS) were quantified using 2′,7′-dichlorofluorescein diacetate. Cell migration was evaluated using Transwell assays. Contractile activity was measured by collagen contraction assay; (3) Results: 4-PBA inhibited TGF-β1 or TG-induced ER-stress marker expression, phenotypic changes, and ECM. Pre-treatment with ROS scavengers inhibited the expression of TGF-β1-induced ER-stress markers. Migration and collagen contraction of TGF-β1 or TG-stimulated fibroblasts were ameliorated by 4-PBA treatment. These findings were confirmed in ex vivo organ cultures; (4) Conclusions: 4-PBA downregulates TGF-β1-induced ER-stress marker expression, migration, and collagen contraction via ROS in fibroblasts and organ cultures. These results suggest that ER-stress may play an important role in progression of chronic upper airway inflammatory diseases by aiding pathological tissue remodeling.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%