Yun Jong Lee
Seoul National University · 医学
研究室紹介
Professor Yun Jong Lee's research lab specializes in molecular and cellular mechanisms underlying osteoarthritis and inflammatory myopathies, with a focus on identifying key signaling pathways and biomarkers involved in cartilage degradation and systemic inflammation. The lab investigates the roles of adipokines, innate immune sensors like PKR and TLR3, and transcription factors such as C/EBPβ and SOCS1 in regulating catabolic and inflammatory responses in chondrocytes. Additionally, the lab explores genetic susceptibility factors, particularly VEGF polymorphisms, in steroid-induced osteonecrosis, aiming to uncover novel therapeutic targets. Their work bridges basic molecular mechanisms with clinical applications in musculoskeletal diseases.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15INTRODUCTION: Adiponectin has been implicated in the pathogenesis of osteoarthritis (OA). We studied the effects of adiponectin on the OA cartilage homeostasis. METHODS: Immunohistochemical analysis was performed to evaluate differential expression of adiponectin receptors (AdipoRs) in nonlesional and lesional areas of OA cartilage. Cartilage and chondrocytes from the knee joints of primary OA patients were cultured in the presence of adiponectin (0~30 μg/ml). The levels of total nitric oxide (N
Recent studies have suggested that neutrophil-to-lymphocyte ratio (NLR) and C-reactive protein-to-albumin ratio (CAR) are emerging markers of disease activity and prognosis in patients with chronic inflammatory diseases, cardiovascular diseases, or malignancies. Therefore, we investigated the clinical significance and prognostic value of the NLR and CAR in adult patients with polymyositis and dermatomyositis. The medical records of 197 patients with newly diagnosed polymyositis/dermatomyositis b
Protein kinase R (PKR) is an immune response protein that becomes activated by double-stranded RNAs (dsRNAs). PKR overactivation is associated with degenerative diseases with inflammation, including osteoarthritis (OA), but the dsRNA activator remains largely unknown. Here, we find that mitochondrial dsRNA (mt-dsRNA) expression and its cytosolic efflux are facilitated in chondrocytes under OA-eliciting conditions, leading to innate immune activation. Moreover, mt-dsRNAs are released to the extra
CAAT/enhancer-binding protein-beta (C/EBPβ) is a transcription factor that regulates interleukin-1β (IL-1β)-induced catabolic pathways, including the expression of matrix metalloproteinases (MMPs), in chondrocytes. We previously reported that suppressor of cytokine signaling 1 (SOCS1) inhibits IL-1β signaling in chondrocytes. However, the effect of SOCS1 on C/EBPβ has not been explored. To investigate the interaction between SOCS1 and C/EBPβ, we established human SW1353 cells with overexpression
No pharmacological prevention or treatment of osteonecrosis is recommendable at this moment.
To investigate an association between steroid-induced femoral head osteonecrosis (FHON) and functional vascular endothelial growth factor (VEGF) gene (-2578A/C, -1154A/G, -634C/G, and +405C/G) polymorphisms polymerase chain reaction-restriction fragment length polymorphism genotyping was performed in 160 patients (86 idiopathic FHON and 74 steroid-induced FHON) and 160 gender- and age-matched controls. The steroid-induced subgroup had a significantly lower prevalence of -1154A allele (7.4% vs. 1
Sjӧgren's syndrome (SS) is a systemic autoimmune disease that targets the exocrine glands, resulting in impaired saliva and tear secretion. To date, type I interferons (I-IFNs) are increasingly recognized as pivotal mediators in SS, but their endogenous drivers have not been elucidated. Here, we investigate the role of mitochondrial double-stranded RNAs (mt-dsRNAs) in regulating I-IFNs and other glandular phenotypes of SS. We find that mt-dsRNAs are elevated in the saliva and tears of SS patient
Objectives: This study investigated the expression of proviral-integration site for Moloney murine leukaemia virus (PIM) -1 kinase in RA synovium and RA fibroblast-like synoviocytes (FLSs) along with its impact on RA-FLS aggressiveness. Methods: The expression of PIM kinases was assessed in synovial tissues by immunohistochemistry and double IF. After PIM-1 inhibition using either small-interfering RNA or the chemical inhibitor AZD1208, we performed proliferation and migration assays and measure