Yong‐Sun Maeng
Yonsei University · 医学
研究室紹介
Professor Yong-Sun Maeng's research lab focuses on vascular biology and regenerative medicine, with a central emphasis on endothelial progenitor cells (EPCs), angiogenesis, and lymphangiogenesis in both developmental and pathological contexts. The lab investigates molecular mechanisms regulating EPC homing, differentiation, and vascular barrier function, particularly through growth factor systems (e.g., IGF2/IGF2R), extracellular matrix proteins (e.g., TGFBIp), and epigenetic regulators (e.g., HP1α). Key research directions include understanding the role of TGFBIp in corneal wound healing and ocular surface protection, as well as exploring therapeutic strategies targeting lymphangiogenesis to inhibit cancer metastasis. The lab integrates in vitro cell biology with in vivo disease models to identify novel targets for treating vascular disorders, diabetes-related complications, and cancer.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15Homing of endothelial progenitor cells (EPCs) to the neovascular zone is now considered to be an essential step in the formation of vascular networks during embryonic development and also for neovascularization in postnatal life. We report here the prominent role of the insulin-like growth factor 2 (IGF2)/IGF2 receptor (IGF2R) system in promoting EPC homing. With high-level expression of IGF2R in EPCs, IGF2-induced hypoxic conditions stimulated multiple steps of EPC homing in vitro and promoted
Metastasis is the main cause of mortality in cancer patients. Although there are many anti-cancer drugs targeting tumor growth, anti-metastatic agents are rarely developed. Angiogenesis and lymphangiogenesis are crucial for cancer progression; in particular, lymphangiogenesis is pivotal for metastasis in cancer. Here we report that lithium inhibits colon cancer metastasis by blocking lymphangiogenesis. Lithium reduces the expression of transforming growth factor-β-induced protein (TGFBIp) in col
Endothelial barrier integrity is essential for vascular homeostasis and increased vascular permeability and has been implicated in many pathological processes, including diabetic retinopathy. Here, we investigated the effect of Rk1, a ginsenoside extracted from sun ginseng, on regulation of endothelial barrier function. In human retinal endothelial cells, Rk1 strongly inhibited permeability induced by VEGF, advanced glycation end-product, thrombin, or histamine. Furthermore, Rk1 significantly re
Endothelial progenitor cells (EPCs) in the circulatory system have been suggested to maintain vascular homeostasis and contribute to adult vascular regeneration and repair. These processes require that EPCs recognize the extracellular matrix (ECM), migrate, differentiate, and undergo tube morphogenesis. The ECM plays a critical role by providing biochemical and biophysical cues that regulate cellular behavior. Here, we tested the importance of transforming growth factor-beta-induced protein (TGF
Our findings demonstrate that the locally generated TGFBIp in the cornea may contribute to wound healing of CECs by enhancing the migration, adhesion, and proliferation of CECs. In addition, our results suggest that TGFBIp has a protective effect on ocular surfaces by inducing the expression of mucin genes in corneal and conjunctival epithelial cells. These data suggest that TGFBIp is a useful therapeutic target for patients with corneal wounds.
As the ability to control the differentiation of endothelial stem/progenitor cells (EPCs) into vascular endothelial cell lineages could be useful for promoting neovascularization, it is important to obtain a deeper understanding of the epigenetic mechanisms that regulate EPC differentiation and neovascularization. Heterochromatin protein 1α (HP1α) is known to be involved in the epigenetic regulation of gene silencing. However, recent reports demonstrate that HP1α can also activate gene expressio
Taken together, the results show the functional role of H3K4me in TGFβ1-mediated TGFBIp and ECM gene expression in corneal fibroblasts. Pharmacologic and other therapies that regulate these modifications could have potential cornea-protective effects for granular corneal dystrophy.
Homeostasis and regeneration of corneal epithelia are sustained by limbal epithelial stem cells (LESCs); thus, an LESC deficiency is a major cause of blindness worldwide. Despite the generally promising results of cultivated LESC transplantation, it has been limited by variations in long-term success rates, the use of xenogeneic and undefined culture components, and a scarcity of donor tissues. In this study, we identified the culture conditions required to expand LESCs in vitro and established
Preeclampsia is a syndrome characterized by deterioration of either the maternal condition or the fetal condition. The adverse intrauterine environment made by preeclampsia results into intrauterine growth restriction and increased risk of a variety of diseases in future life. Given the adverse environment of fetal circulation made in the preeclamptic condition, and the role of mesenchymal stem cell (MSC) as a multipotent progenitor cell, we hypothesized that MSCs derived from human umbilical co
The abnormal development or disruption of the lymphatic vasculature has been implicated in metabolic and hypertensive diseases. Recent evidence suggests that the offspring exposed to preeclampsia (PE) in utero are at higher risk of long-term health problems, such as cardiovascular and metabolic diseases in adulthood, owing to in utero fetal programming. We aimed to investigate lymphangiogenic activities in the lymphatic endothelial progenitor cells (LEPCs) of the offspring of PE. Human umbilical
Maternal hyperglycemia, induced by gestational diabetes mellitus (GDM), has detrimental effects on fetal vascular development, ultimately increasing the risk of cardiovascular diseases in offspring. The potential underlying mechanisms through which these complications occur are due to functional impairment and epigenetic changes in fetal endothelial progenitor cells (EPCs), which remain less defined. We confirm that intrauterine hyperglycemia leads to the impaired angiogenic function of fetal EP
<b>Purpose</b>: The function of Solcoseryl in the corneal epithelium has not been fully examined. Here, we investigated the roles of Solcoseryl in the regulation of gene expression and corneal epithelial cell (CEC) activity.<b>Materials and Methods</b>: The effect of Solcoseryl on CEC activity was analyzed through cell migration, adhesion, proliferation, and wound healing assays. Analysis of gene expression was conducted via western blotting and quantitative reverse transcription polymerase chai