Mi Jeong Lee
Seoul National University · 医学
研究室紹介
Professor Mi Jeong Lee's research lab focuses on the biology and therapeutic potential of adipose-derived stem cells (ASCs) and their secretome in metabolic and neurodegenerative diseases. The lab investigates the molecular mechanisms regulating adipogenesis, adipokine secretion, and vitamin D metabolism in human adipose tissue, with a particular emphasis on how inflammation and hormonal signals influence tissue homeostasis. Key research directions include the role of ASC-derived exosomes in modulating pathological phenotypes in Huntington’s disease and the identification of paracrine factors that mediate tissue repair and metabolic regulation.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15Adipose tissue undergoes a continuous remodeling process that normally maintains tissue health, but may spin out of control and lead to adipocyte death in association with the recruitment and activation of macrophages, and systemic insulin resistance.
Human adipose tissue-derived mesenchymal stem cells (hASCs) are useful for regeneration of inflamed or injured tissues. To identify secreted hASC proteins during inflammation, hASCs were exposed to tumor necrosis factor-alpha (TNF-alpha) and conditioned media derived from hASCs were analyzed by liquid chromatography coupled with tandem mass spectrometry. We identified 187 individual proteins as secreted proteins (secretome) in hASC-conditioned media; 118 proteins were secreted at higher levels u
1,25(OH)(2)D(3) inhibits adipogenesis in mouse 3T3-L1 adipocytes, but little is known about its effects or local metabolism in human adipose tissue. We showed that vitamin D receptor (VDR) and 1α-hydroxylase (CYP27B1), the enzyme that activates 25(OH)D(3) to 1,25(OH)(2)D(3), were expressed in human adipose tissues, primary preadipocytes and newly-differentiated adipocytes. Preadipocytes and newly-differentiated adipocytes were responsive to 1,25(OH)(2)D(3), as indicated by a markedly increased e
This review summarizes recent advances in our understanding of the pre- and posttranscriptional mechanisms that regulate leptin production and secretion in adipocytes. Basal leptin production is proportional to the status of energy stores, i.e., fat cell size, and this is mainly regulated by alterations in leptin mRNA levels. Leptin mRNA levels are regulated by hormones, including glucocorticoids and catecholamines, but little is known about the transcriptional mechanisms involved. Leptin synthe
Glucocorticoids (GC) are powerful regulators of adipocyte differentiation, metabolism, and endocrine function and promote the development of upper body obesity, especially visceral fat stores. To provide a comprehensive understanding of how GC affect adipose tissue and adipocyte function, we analyzed patterns of gene expression (HG U95 Affymetrix arrays) after culture of abdominal subcutaneous (Abd sc) and omental (Om) adipose tissues from severely obese subjects (3 F, 1 M) in the presence of in
Serum leptin levels are upregulated in proportion to body fat and also increase over the short term in response to meals or insulin. To understand the mechanisms involved, we assessed leptin synthesis and secretion in samples of adipose tissue from subjects with a wide range of BMI. Tissue leptin content and relative rates of leptin biosynthesis, as determined by metabolic labeling, were highly correlated with each other and with BMI and fat cell size. To understand mechanisms regulating leptin
Men and women are different in their fat mass and distribution pattern. The gynoid-type fat distribution, accumulation in lower-body, is considered to be protective while the android-type accumulation in upper-body, both in abdominal subcutaneous and visceral depots, is detrimental. Sex-dependent depot differences in adipose metabolic and endocrine functions are thought to contribute to the sexual disparity in fat distribution as well as its association with cardiometabolic risks. Although molec
Lysophosphatidic acid (LPA) is elevated in ascites of ovarian cancer patients and is involved in growth and invasion of ovarian cancer cells. Accumulating evidence suggests a pivotal role of mesenchymal stem cells (MSCs) or stromal cells in tumorigenesis. In the present study, we demonstrated that ascites from ovarian cancer patients and LPA increased migration of human MSCs. The migration of MSCs induced by LPA and malignant ascites was completely abrogated by pretreatment with Ki16425, an anta
OBJECTIVE: Our main objective was to compare the regulation of cortisol production within omental (Om) and abdominal subcutaneous (Abd sc) human adipose tissue. METHODS AND PROCEDURES: Om and Abd sc adipose tissue were obtained at surgery from subjects with a wide range of BMI. Hydroxysteroid dehydrogenase (HSD) activity ((3)H-cortisone and (3)H-cortisol interconversion) and expression were measured before and after organ culture with insulin and/or dexamethasone. RESULTS: Type 1 HSD (HSD1) mRNA
Adipose stromal cells proliferate and differentiate into adipocytes, providing a valuable model system for studies of adipocyte biology. We compared differentiation protocols for human preadipocytes and report on their metabolic phenotypes. By simply prolonging the adipogenic induction period from the first 3 to 7 days, the proportion of cells acquiring adipocyte morphology increased from 30-70% to over 80% in human subcutaneous preadipocytes (passages 5-6). These morphological changes were acco