High Mobility Group Box Chromosomal Protein-1 Induces Myofibroblast Differentiation and Extracellular Matrix Production via RAGE, p38, JNK and AP-1 Signaling Pathways in Nasal Fibroblasts
- Authors
- Lee, Soo-Hyung; Cho, Jae Hoon; Park, Joo Hoo; Cho, Jung-Sun; Lee, Heung-Man
- Issue Date
- Nov-2021
- Publisher
- SAGE Publications Inc.
- Keywords
- chronic rhinosinusitis; extracellular matrix; HMGB1; myofibrblast; nasal fibroblast; RAGE
- Citation
- American Journal of Rhinology and Allergy, v.35, no.6, pp 774 - 780
- Pages
- 7
- Indexed
- SCIE
SCOPUS
- Journal Title
- American Journal of Rhinology and Allergy
- Volume
- 35
- Number
- 6
- Start Page
- 774
- End Page
- 780
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/52000
- DOI
- 10.1177/1945892421998142
- ISSN
- 1945-8924
1945-8932
- Abstract
- Background: Chronic rhinosinusitis is involved in myofibroblast differentiation and extracellular matrix (ECM) accumulation. High mobility group box chromosomal protein 1 (HMGB-1) is known to stimulate lung fibroblast to produce ECM in lung fibrosis. The aim of this study was to investigate whether HMGB-1 induces myofibroblast differentiation and ECM production in nasal fibroblasts and to identify the signal pathway. Methods: Human nasal fibroblasts were cultured. After stimulation with HMGB-1, expressions of α-smooth muscle actin (α-SMA) and fibronectin were determined by real-time PCR and western blot. Total collagen was measured by Sircol assay. To investigate signal pathway, various signal inhibitors and RAGE siRNA were used. Results: HMGB-1 increased α-SMA and fibronectin in mRNA and protein levels. It also increased collagen production. RAGE siRNA inhibited HMGB-1-induced α-SMA and fibronectin, and production of collagen. Furthermore, the inhibitors of RAGE downstream molecules such as p38, JNK and AP-1 also blocked the HMGB-1-induced effects. Conclusions: HMGB-1 induces myofibroblast differentiation and ECM production in nasal fibroblast, which is mediated by RAGE, p38, JNK and AP-1 signal pathway. These results suggest that HMGB-1 may play an important role in tissue remodeling during chronic rhinosinusitis progression. © The Author(s) 2021.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - 2. Clinical Science > Department of Otorhinolaryngology-Head and Neck Surgery > 1. Journal Articles
- 4. Research institute > Institute for Medical Device Clinical Trial > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.