Jaemin Shin
Korea University · Medicine
About the Lab
Professor Jaemin Shin's research lab focuses on the molecular mechanisms underlying tissue remodeling in chronic upper airway inflammatory diseases, particularly chronic rhinosinusitis and nasal polyposis. The lab investigates key pathways involved in fibroblast activation, extracellular matrix deposition, endoplasmic reticulum stress, and angiogenesis, with a strong emphasis on transforming growth factor-beta (TGF-β) signaling and its modulation by pharmacological agents such as pirfenidone, doxycycline, and cigarette smoke extract. Current research also explores the role of cellular proliferation and aging in disease progression and treatment outcomes, aiming to identify novel therapeutic targets for fibrotic and inflammatory airway disorders.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15PURPOSE: Pirfenidone has been shown to have antifibrotic and anti-inflammatory effects in the lungs. The purpose of this study was to evaluate the inhibitory effects of pirfenidone on transforming growth factor (TGF)-β1-induced myofibroblast differentiation and extracellular matrix accumulation. We also determined the molecular mechanisms of pirfenidone in nasal polyp-derived fibroblasts (NPDF). METHODS: NPDFs were isolated from nasal polyps from eight patients who had chronic rhinosinusitis wit
Chronic rhinosinusitis (CRS) is a multifactorial inflammatory disease of the nose and sinuses that affects more than 10% of the adult population worldwide. Currently, CRS is classified into endotypes according to the inflammatory response (Th1, Th2, and Th17) or the distribution of immune cells in the mucosa (eosinophilic and non-eosinophilic). CRS induces mucosal tissue remodeling. Extracellular matrix (ECM) accumulation, fibrin deposition, edema, immune cell infiltration, and angiogenesis are
(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-ph
PURPOSE: Cigarette smoke is a complex mixture of various chemical compounds, including free radicals and highly toxic compounds. Cigarette smoke exposure has been shown to be associated with chronic rhinosinusitis and tissue remodeling in upper airway. Vascular endothelial growth factor (VEGF) is one of the cytokines with a crucial role in tissue remodeling of airway. The aims of this study were to determine the effects of cigarette smoke extract (CSE) on VEGF expression and to investigate the u
PURPOSE: It is well known that doxycycline has antibacterial and anti-inflammatory effects. In this study, we aimed to investigate the effects of doxycycline on the transforming growth factor (TGF) beta 1-induced matrix metalloproteinase (MMP) 2 expression, migration, and collagen contraction, and to determine its molecular mechanism on nasal polyp-derived fibroblasts (NPDF). METHODS: NPDFs were isolated from the nasal polyps of six patients. Doxycycline was used to pretreat TGF-beta-1-induced N
BACKGROUND: Cellular proliferation and angiogenesis are associated with pathophysiology of nasal polyposis (NP). In a previous report, we showed that patient age is a predictive factor of surgical outcomes among patients with chronic rhinosinusitis and NP, and that geriatric patients exhibit better outcomes than pediatric and adult patients. We postulated that better outcomes in the geriatric population may be secondary to decreased proliferation and angiogenesis within polyps. Therefore, we eva
Tissue remodeling contributes to ongoing inflammation and refractoriness of chronic rhinosinusitis (CRS). During this process, epithelial-mesenchymal transition (EMT) plays an important role in dysregulated remodeling and both microRNA (miR)-29b and heat shock protein 47 (HSP47) may be engaged in the pathophysiology of CRS. This study aimed to determine the role of miR-29b and HSP47 in modulating transforming growth factor (TGF)-β1-induced EMT and migration in airway epithelial cells. Expression
Purpose Methyl-CpG-binding protein 2 (MeCP2), known as a transcriptional regulator, has been suggested to play an important role in myofibroblast differentiation in the lung. The purpose of this study was to investigate the role of MeCP2 in transforming growth factor (TGF)- β1-induced myofibroblast differentiation and extracellular matrix (ECM) production in nasal polyp-derived fibroblasts (NPDFs). Methods To identify the expression of MeCP2 in nasal polyp tissues, immunohistochemistry staining
BACKGROUND: Doxycycline has been shown to have antibacterial and anti-inflammatory effects and suppresses collagen biosynthesis. The purpose of this study was to evaluate the effects of doxycycline on transforming growth factor (TGF)-β1-induced myofibroblast differentiation and extracellular matrix production in nasal polyp-derived fibroblasts (NPDFs). We also determined the molecular mechanisms of action for doxycycline. METHODS: NPDFs were isolated from nasal polyps from 8 patients. Doxycyclin
We showed that baicalin down-regulated myofibroblast differentiation, extracellular matrix production, migration, and collagen contraction via the MAPK and Akt/ NF-κB pathways in IL-1β-stimulated nasal fibroblasts.
Deficiencies in epithelial barrier integrity are involved in the pathogenesis of chronic rhinosinusitis (CRS). This study aimed to investigate the role of ephrinA1/ephA2 signaling on sinonasal epithelial permeability and rhinovirus-induced epithelial permeability. This role in the process of epithelial permeability was evaluated by stimulating ephA2 with ephrinA1 and inactivating ephA2 with ephA2 siRNA or inhibitor in cells exposed to rhinovirus infection. EphrinA1 treatment increased epithelial
BACKGROUND: Glycolytic reprogramming is a key feature of chronic inflammatory disease. Extracellular matrix (ECM) produced by myofibroblasts plays an important role in tissue remodeling of nasal mucosa in chronic rhinosinusitis (CRS). This study aimed to determine whether glycolytic reprogramming contributes to myofibroblast differentiation and ECM production in nasal fibroblasts. METHODS: Primary nasal fibroblasts were isolated from the nasal mucosa of patients with CRS. Glycolytic reprogrammin
PURPOSE: Doxycycline has antibacterial and anti-inflammatory effects, and it also suppresses collagen biosynthesis. This study aimed to confirm the effects and mechanism of doxycycline on transforming growth factor (TGF) beta 1 induced epithelial-mesenchymal transition and cell migration in A549 and primary nasal epithelial cells. METHODS: A 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay and phalloidin-fluorescein isothiocyanate staining were used to evaluate cytotoxicity and
The lengths of the actual SBDs were longer than those of anticipated SBDs in all patients, while the width of actual SBDs showed less discrepancy. Length and anterior width of the potential SF exceeded the needed SF dimensions in two patients, while the posterior width of potential SF fell short of the needed dimension. In both patients, the length of harvested SF was long enough to repair the entire length of SBD, while shortage of SF width was encountered in one patient.
Research Areas
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