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Park, Gyuman,Yoon, Byung Sun,Moon, Jai-Hee,Kim, Bona,Jun, Eun Kyoung,Oh, Sejong,Kim, Hyunggee,Song, Hea Joon,Noh, Joo Young,Oh, ChilHwan,You, Seungkwon The Society for Investigative Dermatology, Inc 2008 The Journal of investigative dermatology Vol.128 No.10
Keloids are benign skin tumors characterized by collagen accumulation and hyperproliferation of fibroblasts. To find an effective therapy for keloids, we explored the pharmacological potential of (−)-epigallocatechin-3-gallate (EGCG), a widely investigated tumor-preventive agent. When applied to normal and keloid fibroblasts (KFs) in vitro, proliferation and migration of KFs were more strongly suppressed by EGCG than normal fibroblast proliferation and migration (IC<SUB>50</SUB>: 54.4 μM (keloid fibroblast (KF)) versus 63.0 μM (NF)). The level of Smad2/3, signal transducer and activator of transcription-3 (STAT3), and p38 phosphorylation is more enhanced in KFs, and EGCG inhibited phosphorylation of phosphatidylinositol-3-kinase (PI3K), extracellular signal-regulated protein kinase 1/2 (ERK1/2), and STAT3 (Tyr705 and Ser727). To evaluate the contribution of these pathways to keloid pathology, we treated KFs with specific inhibitors for PI3K, ERK1/2, or STAT3. Although a PI3K inhibitor significantly suppressed proliferation, PI3K and MEK/ERK inhibitors had a minor effect on migration and collagen production. However, a JAK2/STAT3 inhibitor and a STAT3 siRNA strongly suppressed proliferation, migration, and collagen production by KFs. We also found that treatment with EGCG suppressed growth and collagen production in the in vivo keloid model. This study demonstrates that EGCG suppresses the pathological characteristics of keloids through inhibition of the STAT3-signaling pathway. We propose that EGCG has potential in the treatment and prevention of keloids.Journal of Investigative Dermatology (2008) 128, 2429–2441; doi:10.1038/jid.2008.103; published online 8 May 2008
WDNM1 is associated with differentiation and apoptosis of mammary epithelial cells.
Kho, Yoonjung,Kim, Sungchan,Yoon, Byung Sun,Moon, Jai-Hee,Kwak, Sungwook,Park, Gyuman,Woo, Junghee,Oh, Sejong,Hong, Kichang,Kim, Saehun,Kim, Hyunggee,You, Seungkwon,Choi, Yunjaie Marcel Dekker 2008 Animal biotechnology Vol.19 No.2
<P>In this study, we show that expression of the Westmead DMBA8 nonmetastatic cDNA 1 (WDNM1) gene was increased upon SFM and/or TNFalpha treatment, with a corresponding increase in apoptotic cells, and gradually decreased following re-stimulation with serum in HC11 mammary epithelial cells. TNFalpha induced WDNM1 expression showed the NFkappaB-dependent mechanism since it's expression was abrogated in IkappaBalphaM (super-repressor of NFkappaB)-transfected cells, but not those transfected with control vector. Furthermore, overexpression of WDNM1 suppressed growth and differentiation, and accelerated apoptosis of HC11 cells. Thus, our results demonstrate that WDNM1 gene expression, regulated by the TNFalpha-NFkappaB signal pathway, is associated with HC11 cell apoptosis.</P>
Design and Fabrication of a PDMS/Parylene Microvalve for the Treatment of Hydrocephalus
Jonghyun Oh,Gyuman Kim,Kralick, F.,Hongseok Noh IEEE 2011 Journal of microelectromechanical systems Vol.20 No.4
<P>We present a novel microvalve for the treatment of a pathological condition, i.e., hydrocephalus. This microvalve is made of polydimethylsiloxane/Parylene composite layer which has a 3-D dome petal shape. This geometry enables the microvalve to rectify fluid flow in the forward and backward directions. New microfabrication techniques such as dome-shaped SU-8 mold fabrication and excimer laser machining for valve opening have been investigated to build the proposed microvalve. The pressure drop versus flow rate characteristics of the fabricated microvalve was investigated through in vitro flow tests. The flow test results showed that a 10 × 10 microvalve array with a cross-cut opening shape (200 × 60 μm) was found to be optimal for the treatment of hydrocephalus.</P>
Human induced neural stem cells support functional recovery in spinal cord injury models
Son Daryeon,Zheng Jie,Kim In Yong,Kang Phil Jun,Park Kyoungmin,Priscilla Lia,Hong Wonjun,Yoon Byung Sun,Park Gyuman,Yoo Jeong-Eun,Song Gwonhwa,Lee Jang-Bo,You Seungkwon 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Spinal cord injury (SCI) is a clinical condition that leads to permanent and/or progressive disabilities of sensory, motor, and autonomic functions. Unfortunately, no medical standard of care for SCI exists to reverse the damage. Here, we assessed the effects of induced neural stem cells (iNSCs) directly converted from human urine cells (UCs) in SCI rat models. We successfully generated iNSCs from human UCs, commercial fibroblasts, and patient-derived fibroblasts. These iNSCs expressed various neural stem cell markers and differentiated into diverse neuronal and glial cell types. When transplanted into injured spinal cords, UC-derived iNSCs survived, engrafted, and expressed neuronal and glial markers. Large numbers of axons extended from grafts over long distances, leading to connections between host and graft neurons at 8 weeks post-transplantation with significant improvement of locomotor function. This study suggests that iNSCs have biomedical applications for disease modeling and constitute an alternative transplantation strategy as a personalized cell source for neural regeneration in several spinal cord diseases.
Glycine decarboxylase regulates the maintenance and induction of pluripotency via metabolic control
Kang, Phil Jun,Zheng, Jie,Lee, Gilju,Son, Daryeon,Kim, In Yong,Song, Gwonhwa,Park, Gyuman,You, Seungkwon Academic Press 2019 Metabolic engineering Vol.53 No.-
<P><B>Abstract</B></P> <P>Reprogramming of ‘adult’ differentiated somatic cells to ‘embryonic’ pluripotent stem cells accompanied by increased rate of glycolysis. Conversely, glycolysis triggers accumulation of advanced glycation end products (AGEs), a potential causative factor in aging, by promoting methylglyoxal production. Therefore, it is reasonable that pluripotent stem cells (PSCs) would specifically regulate glycolysis to maintain their embryonic features. In this study, we focused on glycine decarboxylase (GLDC), a key enzyme in the glycine cleavage system that regulates glycolysis and methylglyoxal production in cancer. GLDC was exclusively expressed in PSCs, and inhibition of this enzyme induced alterations of metabolome and AGE accumulation, thereby suppressing the embryonic pluripotent state. Surprisingly, the level of accumulated AGEs in somatic cells gradually decreased during reprogramming, ultimately disappearing in iPSCs. In addition, ectopic expression of GLDC or treatment with the AGE inhibitor LR-90 promoted reprogramming. Together, these findings suggest that GLDC-mediated regulation of glycolysis and controlling AGE accumulation is related to maintenance and induction of pluripotency.</P> <P><B>Highlights</B></P> <P> <UL> <LI> GLDC is a metabolic regulator in human PSCs. </LI> <LI> GLDC-mediated regulation of glycolysis is involved in controlling AGE accumulation. </LI> <LI> AGE depletion is related to maintenance and induction of pluripotency. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Jun, Eun Kyoung,Zhang, Qiankun,Yoon, Byung Sun,Moon, Jai-Hee,Lee, Gilju,Park, Gyuman,Kang, Phil Jun,Lee, Jung Han,Kim, Areee,You, Seungkwon Molecular Diversity Preservation International (MD 2014 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.15 No.1
<P>In a previous study, we isolated human amniotic fluid (AF)-derived mesenchymal stem cells (AF-MSCs) and utilized normoxic conditioned medium (AF-MSC-norCM) which has been shown to accelerate cutaneous wound healing. Because hypoxia enhances the wound healing function of mesenchymal stem cell-conditioned medium (MSC-CM), it is interesting to explore the mechanism responsible for the enhancement of wound healing function. In this work, hypoxia not only increased the proliferation of AF-MSCs but also maintained their constitutive characteristics (surface marker expression and differentiation potentials). Notably, more paracrine factors, VEGF and TGF-β1, were secreted into hypoxic conditioned medium from AF-MSCs (AF-MSC-hypoCM) compared to AF-MSC-norCM. Moreover, AF-MSC-hypoCM enhanced the proliferation and migration of human dermal fibroblasts <I>in vitro</I>, and wound closure in a skin injury model, as compared to AF-MSC-norCM. However, the enhancement of migration of fibroblasts accelerated by AF-MSC-hypoCM was inhibited by SB505124 and LY294002, inhibitors of TGF-β/SMAD2 and PI3K/AKT, suggesting that AF-MSC-hypoCM-enhanced wound healing is mediated by the activation of TGF-β/SMAD2 and PI3K/AKT. Therefore, AF-MSC-hypoCM enhances wound healing through the increase of hypoxia-induced paracrine factors via activation of TGF-β/SMAD2 and PI3K/AKT pathways.</P>