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Open AccessArticle

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

by Jae-Min Shin 1,2,†, Ju-Hyung Kang 1,†, Joo-Hoo Park 1,2, Hyun-Woo Yang 1,2, Heung-Man Lee 1,2 and Ii-Ho Park 1,2,*
1
Upper Airway Chronic Inflammatory Diseases Laboratory, Korea University College of Medicine, Seoul 08308, Korea
2
Department of Otorhinolaryngology-Head and Neck Surgery, Korea University College of Medicine, Seoul 08308, Korea
*
Author to whom correspondence should be addressed.
These authors contributed equally to this study.
Biomolecules 2020, 10(6), 942; https://doi.org/10.3390/biom10060942
Received: 3 March 2020 / Revised: 18 June 2020 / Accepted: 19 June 2020 / Published: 22 June 2020
(This article belongs to the Special Issue Endoplasmic Reticulum Stress in Diseases)
(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. View Full-Text
Keywords: transforming growth factor beta-1; unfolded protein response; extracellular matrix; airway remodeling; nose; fibroblast transforming growth factor beta-1; unfolded protein response; extracellular matrix; airway remodeling; nose; fibroblast
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Shin, J.-M.; Kang, J.-H.; Park, J.-H.; Yang, H.-W.; Lee, H.-M.; Park, I.-H. TGF-β1 Activates Nasal Fibroblasts through the Induction of Endoplasmic Reticulum Stress. Biomolecules 2020, 10, 942.

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