Seoul National University · 医学
Professor Je Kyung Seong's research lab focuses on molecular and systems biology approaches to understand the pathophysiology of chronic inflammatory diseases and metabolic disorders. The lab investigates mucin dysregulation in airway diseases such as nasal polyps, oxidative stress adaptation mechanisms in immune cells, and the role of lipid metabolism—particularly plasmalogens and lysophospholipids—in obesity-related metabolic dysfunction. Key research directions include proteomic and lipidomic profiling to identify novel therapeutic targets in atherosclerosis, metabolic syndrome, and chronic inflammation. The lab integrates multi-omics technologies with in vivo and in vitro models to dissect disease mechanisms and signaling pathways.
Figures are computed from collected data and may differ slightly.
Polyps are believed to be the source of mucus hypersecretion in chronic inflammation of the sinus. However, it is not clear which mucins are responsible for the hypersecretion of mucus by nasal polyps. We describe the over-expression of MUC8 mRNA in nasal polyps and the upregulation of MUC8 mRNA expression and downregulation of MUC5AC mRNA expression by inflammatory mediators. We found that the level of MUC8 mRNA, but not the level of MUC5AC mRNA, increased in nasal polyps. We also found that th
When cells are first exposed to low levels of oxidative stress, they develop a resistance to a subsequent challenge of the same stress, even at higher levels. Although some protein(s) induced by oxidative stress likely mediated this adaptive response, the nature of these proteins is unknown. In this study, the total proteins extracted from human U937 leukemia cells exposed to 50 micromM H(2)O(2) for 24 h to induce an optimal protective response were analyzed by two-dimensional polyacrylamide gel
We report here a proteomic analysis of differentially expressed liver proteins of both C57BL/6J (B6, atherosclerosis-susceptible strain) and C3H/HeJ mice (C3H, atherosclerosis-resistant strain), which were fed either control or a high-fat enriched atherogenic diet for eight weeks. We observed differential patterns of plasma lipids between the two strains when both were fed atherogenic diets. That is, although low density lipoprotein cholesterol level was highly elevated in both, the levels of to
Dysregulation of adipose tissue plasmalogen metabolism is associated with obesity-related metabolic diseases. We report that feeding mice a high-fat diet reduces adipose tissue lysoplasmalogen levels and increases transmembrane protein 86 A (TMEM86A), a putative lysoplasmalogenase. Untargeted lipidomic analysis demonstrates that adipocyte-specific TMEM86A-knockout (AKO) increases lysoplasmalogen content in adipose tissue, including plasmenyl lysophosphatidylethanolamine 18:0 (LPE P-18:0). Surpri
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