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Dive into the research topics where Seong-Suk Jue is active.

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Featured researches published by Seong-Suk Jue.


Journal of Pineal Research | 2015

Melatonin promotes hepatic differentiation of human dental pulp stem cells: clinical implications for the prevention of liver fibrosis

Young-Ah Cho; Kwantae Noh; Seong-Suk Jue; So-Youn Lee; Eun-Cheol Kim

Melatonins effect on hepatic differentiation of stem cells remains unclear. The aim of this study was to investigate the action of melatonin on hepatic differentiation as well as its related signaling pathways of human dental pulp stem cells (hDPSCs) and to examine the therapeutic effects of a combination of melatonin and hDPSC transplantation on carbon tetrachloride (CCl4)‐induced liver fibrosis in mice. In vitro hepatic differentiation was assessed by periodic acid‐Schiff (PAS) staining and mRNA expression for hepatocyte markers. Liver fibrosis model was established by injecting 0.5 mL/kg CCl4 followed by treatment with melatonin (5 mg/kg, twice a week) and hDPSCs. In vivo therapeutic effects were evaluated by histopathology and by means of liver function tests including measurement of alanine transaminase (ALT), aspartate transaminase (AST), and ammonia levels. Melatonin promoted hepatic differentiation based on mRNA expression of differentiation markers and PAS‐stained glycogen‐laden cells. In addition, melatonin increased bone morphogenic protein (BMP)‐2 expression and Smad1/5/8 phosphorylation, which was blocked by the BMP antagonist noggin. Furthermore, melatonin activated p38, extracellular signal‐regulated kinase (ERK), and nuclear factor‐κB (NF‐κB) in hDPSCs. Melatonin‐induced hepatic differentiation was attenuated by inhibitors of BMP, p38, ERK, and NF‐κB. Compared to treatment of CCl4‐injured mice with either melatonin or hDPSC transplantation alone, the combination of melatonin and hDPSC significantly suppressed liver fibrosis and restored ALT, AST, and ammonia levels. For the first time, this study demonstrates that melatonin promotes hepatic differentiation of hDPSCs by modulating the BMP, p38, ERK, and NF‐κB pathway. Combined treatment of grafted hDPSCs and melatonin could be a viable approach for the treatment of liver cirrhosis.


Stem Cells and Development | 2014

The role of PIN1 on odontogenic and adipogenic differentiation in human dental pulp stem cells.

Young-Man Lee; Seung-Yun Shin; Seong-Suk Jue; Il-Keun Kwon; Eun-Hee Cho; Eui-Sic Cho; Sang-Hyuk Park; Eun-Cheol Kim

Recently, the involvement of PIN1, a peptidyl-prolyl cis/trans isomerase, has been reported in age-related bone homeostasis and adipogenesis. However, the role of PIN1 during odontogenic and adipogenic differentiation remains to be fully understood, particularly regarding human dental pulp stem cells (HDPSCs). Thus, in the present study, we have investigated the role of PIN1 in odontogenic and adipogenic differentiation of HDPSCs and signaling pathways possibly involved. PIN1 mRNA and protein level were upregulated in a time-dependent manner during adipogenic differentiation, increasing until 1 day of odontogenic induction and then steadily declined during odontogenic differentiation. Treatment of a known PIN1 inhibitor, juglone, significantly increased odontogenic differentiation as confirmed by alkaline phosphatase (ALP) activity, calcium deposition, and mRNAs induction of odontogenic markers [ALP, osteopontin (OPN), osteocalcin (OCN), dentin sialophosphoprotein (DSPP), and dentin matrix protein 1 (DMP-1)]. On the contrary, adipogenic differentiation was dramatically reduced upon juglone treatment, with concomitant downregulation of lipid droplet accumulation and adipogenic marker genes [peroxisome proliferation-activated receptor gamma (PPARγ), lipoprotein lipase (LPL), and adipocyte fatty acid-binding protein (AP2)]. In contrast to PIN1 inhibition, the overexpression of PIN1 via adenoviral infection (Ad-PIN1) in HDPSCs inhibited odontogenic differentiation but increased adipogenic differentiation, in which stem cell property markers such as stage-specific embryonic antigen-4 (SSEA-4) and STRO-1 were upregulated during odontogenic differentiation but downregulated in adiopogenic differentiation. Consistently, juglone-mediated inhibition of PIN1 augmented the osteogenic medium (OM)-induced activation of bone morphogenetic protein (BMP), Wnt/β-catenin, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and nuclear factor-kappa B (NF-κB) pathway, which response was reversed by Ad-PIN1. Moreover, juglone blocked the adipogenic induction medium-induced activation of PPARγ, C/EBPα, C/EBPβ, ERK, and NF-κB pathways, which was rescued by Ad-PIN1 infection. In summary, the present study shows for the first time that PIN1 acts as an important modulator of odontogenic and adipogenic differentiation of HDPSCs and may have clinical implications for regenerative dentistry.


Journal of Neuroscience Research | 2015

Comparison of the effects of human dental pulp stem cells and human bone marrow‐derived mesenchymal stem cells on ischemic human astrocytes in vitro

Miyeoun Song; Seong-Suk Jue; Young-Ah Cho; Eun-Cheol Kim

This study assesses the cytoprotective effects of human dental pulp stem cells (hDPSCs) and conditioned medium from hDPSCs (CM‐hDPSCs) on ischemic human astrocytes (hAs) in vitro compared with human bone marrow‐derived mesenchymal stem cells (hMSCs). Ischemia of hAs was induced by oxygen–glucose deprivation (OGD). CM‐hDPSCs and hMSCs were collected after 48 hr of culture. Cell death was determined by 3‐[4,5‐dimethylthialzol‐2‐yl]‐2,5‐diphenyltetrazolium bromide and cellular ATP assays. The expression of glial fibrillary acidic protein (GFAP) and musashi‐1 as markers of reactive astrogliosis was examined with immunochemical staining. mRNA expression and reactive oxygen species (ROS) were analyzed by RT‐PCR and flow cytometry, respectively. OGD increased cytotoxicity in a time‐dependent manner and decreased cellular ATP content concomitantly in hAs. Pretreatment and posttreatment with hDPSCs were associated with greater recovery from OGD‐induced cytotoxicity in hAs compared with hMSCs. Similarly, CM‐hDPSCs had a greater effect on OGD‐induced cytotoxicity in a dose‐dependent manner. Pre‐ and posttreatment with CM‐hDPSCs or CM‐hMSCs attenuated OGD‐induced GFAP, nestin, and musashi‐1 expression in hAs. Furthermore, treatment of cells with CM‐hDPSCs and hMSCs blocked OGD‐induced ROS production and interleukin‐1ß upregulation. This study demonstrates for the first time that hDPSCs and CM‐hDPSCs confer superior cytoprotection against cell death in an in vitro OGD model compared with hMSCs as shown by cell viability assay. Reactive gliosis, ROS production, and inflammatory mediators might contribute to this protective effect. Therefore, hDPSCs could represent an alternative source of cell therapy for ischemic stroke.


Angle Orthodontist | 2012

Localization of osteopontin and osterix in periodontal tissue during orthodontic tooth movement in rats

Ji-Youn Kim; Byung-In Kim; Seong-Suk Jue; Jae Hyun Park; Je-Won Shin

OBJECTIVE To evaluate the localization of osteopontin (OPN) and osterix in periodontal tissue during experimental tooth movement with heavy force in rats. MATERIALS AND METHODS Nickel-titanium closed-coil springs were used to create a 100 g mesial force to the maxillary first molars. On days 3, 7, 10, and 14 after force application, histological changes in periodontium were examined by immunohistochemistry using proliferating cell nuclear antigen (PCNA), OPN, and osterix. RESULTS PCNA-positive cells were found close to the alveolar bone and cementum on both sides. OPN-positive cells were observed along the cementing line of the cementum and bone on both sides and also were visible along with newly formed fibers in the periodontal ligament on the tension side. Osterix-positive cells were strongly detected on the surface of the alveolar bone and cementum on both sides. CONCLUSIONS During tooth movement, periodontal remodeling occurs on both sides. These results indicate that OPN and osterix may play an important role of differentiation and osteoblasts and cementoblasts matrix formation during periodontal tissue remodeling.


Clinical Oral Implants Research | 2010

The effects of enamel matrix derivative on the proliferation and differentiation of human mesenchymal stem cells

Seong-Suk Jue; Won Young Lee; Yong-Dae Kwon; Young-Ran Kim; Ahran Pae; Baek-Soo Lee

PURPOSE This study was designed to investigate the effect of enamel derivative matrix (EMD) on the proliferation, mineralization, and differentiation of human mesenchymal stem cells (hMSCs). MATERIAL AND METHODS For the proliferation assay, water-soluble tetrazolium salt-8 tests were carried out after culturing for 24 and 48 h. For the evaluation of mineralization, Alizarin red S (ARS) tests were performed after 21 days of culturing in an osteogenic medium. In order to investigate some of the bone-related proteins, namely type I collagen (Col I A2), bone sialoprotein (BSP), and bone gamma-carboxyglutamate (Gla) protein (BGLAP, osteocalcin), real-time polymerase chain reaction (RT-PCR) tests were carried out after 2, 3, and 4 weeks of culturing, respectively. RESULTS The activity of proliferation and mineralization increased significantly depending on the concentration of EMD (P<0.05). In the control group, the expression of Col I A2 decreased, but EMD enhanced its expression over time and was correlated to the concentration. The amount of expression of BSP in this group increased over time, but EMD strikingly suppressed its expression in the fourth week. As well, the amount of expression of BGLAP increased as the culture duration lengthened in the control group. However, the expression of BGLAP was suppressed in the experimental group with EMD. CONCLUSION Within the limits of this study, EMD enhanced the proliferation of hMSCs. After evaluation with ARS staining, EMD seemed to enhance mineralization, and the RT-PCR test revealed that EMD promoted early-stage osteoblast differentiation by enhancing Col I A2 expression, but exerted an inhibitory effect on the mineralization by lowering the gene expression of BSP and BGLAP. Mineralized nodules formed with EMD may be composed of substances other than normal bone. Because most of the organic matrix of bone is type I collagen, which acts as the mineralization site, bone or bone-like mineralized mass might have been formed in spite of the different components of the non-collagenous proteins.


Journal of Dental Research | 2015

PIN1 Inhibition Suppresses Osteoclast Differentiation and Inflammatory Responses

Young-Ah Cho; Seong-Suk Jue; Won-Jung Bae; S.-H. Heo; Seung-Il Shin; Il-Keun Kwon; S.-C. Lee; E.-C. Kim

Inflammatory responses and osteoclast differentiation play pivotal roles in the pathogenesis of osteolytic bone diseases such as periodontitis. Although overexpression or inhibition of peptidyl-prolyl cis/trans isomerase NIMA-interacting 1 (PIN1) offers a possible therapeutic strategy for chronic inflammatory diseases, the role of PIN1 in periodontal disease is unclear. The aim of the present study was to evaluate PIN1 expression in periodontitis patients as well as the effects of PIN1 inhibition by juglone or PIN1 small-interfering RNA (siRNA) and of PIN1 overexpression using a recombinant adenovirus encoding PIN1 (Ad-PIN1) on the inflammatory response and osteoclastic differentiation in lipopolysaccharide (LPS)- and nicotine-stimulated human periodontal ligament cells (PDLCs). PIN1 was up-regulated in chronically inflamed PDLCs from periodontitis patients and in LPS- and nicotine-exposed PDLCs. Inhibition of PIN1 by juglone or knockdown of PIN1 gene expression by siRNA markedly attenuated LPS- and nicotine-stimulated prostaglandin E2 (PGE2) and nitric oxide (NO) production, as well as cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expression, whereas PIN1 overexpression by Ad-PIN1 increased it. LPS- and nicotine-induced nuclear factor (NF)-κB activation was blocked by juglone and PIN1 siRNA but increased by Ad-PIN1. Conditioned medium prepared from LPS- and nicotine-treated PDLCs increased the number of tartrate-resistant acid phosphatase–stained osteoclasts and osteoclast-specific gene expression. These responses were blocked by PIN1 inhibition and silencing but stimulated by Ad-PIN1. Furthermore, juglone and PIN1 siRNA inhibited LPS- and nicotine-induced osteoclastogenic cytokine expression in PDLCs. This study is the first to demonstrate that PIN1 inhibition exhibits anti-inflammatory effects and blocks osteoclastic differentiation in LPS- and nicotine-treated PDLCs. PIN1 inhibition may be a therapeutic strategy for inflammatory osteolysis in periodontal disease.


Journal of Endodontics | 2014

Effects of Glutamine on Proliferation, Migration, and Differentiation of Human Dental Pulp Cells

Duck-Su Kim; Seong-Suk Jue; So-Youn Lee; Young-Suk Kim; Seung-Yun Shin; Eun-Cheol Kim

INTRODUCTION Although glutamine (Gln) is mitogenic in various cell types, little is known about its role in human dental pulp cells (HDPCs). This study investigated the effects of Gln on proliferation, migration, and odontoblastic differentiation of HDPCs and the underlying signal pathway mechanisms. METHODS Growth and migration were assessed by cell counting and colorimetric cell migration kits. Differentiation was measured as alkaline phosphatase activity, calcified nodule formation by alizarin red staining, and marker mRNA expression by reverse transcriptase-polymerase chain reaction (RT-PCR). Chemokine expression was also evaluated by RT-PCR. Signal transduction pathways were examined by RT-PCR and Western blot analysis. RESULTS Gln dose-dependently increased proliferation, migration, alkaline phosphatase activity, mineralized nodule formation, and odontoblast-marker mRNA of HDPCs. Gln also up-regulated expression of interleukin-6, interleukin-8, MCP-1, MIP-3α, CCL2, CCL20, and CXCL1. Gln increased BMP-2 and BMP-4 mRNA, phosphorylation of Smad 1/5/8, β-catenin, and key proteins of the Wnt signaling pathway. Furthermore, Gln resulted in up-regulation of extracellular signal-regulated kinase, p38, and c-Jun N-terminal kinase. In addition, noggin, DKK1, inhibitors of p38, ERK, and JNK significantly attenuatted Gln-induced growth, migration, and odontoblastic differentiation. CONCLUSIONS Collectively, this study demonstrated that Gln promoted growth, migration, and differentiation in HDPCs through the BMP-2, Wnt, and MAPK pathways, leading to improved pulp repair and regeneration.


Angle Orthodontist | 2014

Localization of ODAM, PCNA, and CK14 in regenerating junctional epithelium during orthodontic tooth movement in rats

Seong-Suk Jue; Ji-Youn Kim; Seung-Hoon Na; Kyung-Dal Jeon; Hee-Joon Bang; Jae Hyun Park; Je-Won Shin

OBJECTIVE To identify the regenerating junctional epithelium (JE) during orthodontic tooth movement in rats. MATERIALS AND METHODS Closed-coil springs were used to create a 20 g mesial force to the maxillary first molars. On days 1, 3, 7, 10, and 14 after force application, histologic changes in JE were examined by immunohistochemistry using proliferating cell nuclear antigen (PCNA), odontogenic ameloblast-associated protein (ODAM), and cytokeratin 14 (CK14). RESULTS On day 1, JE was destroyed and lost attachment to the tooth surface. Cell division activity was rarely observed in JE, and ODAM localization was weakly detected in damaged JE. By day 3, regenerating JE had not fully recovered. High cell proliferation activity and CK14 expression started to appear in most basal cells of JE. ODAM expression was reduced and appeared in a small area. By day 7, JE had almost recovered. Cell proliferation activity was still observed in several basal cells of JE, and ODAM expression was detected among JE cells. CK14 was hardly observed in JE except in the basal cells. By days 10 and 14, regenerated JE appeared. ODAM, PCNA, and CK14 expression was similar to that of the control. CONCLUSIONS Damaged JE might recover rapidly during orthodontic tooth movement because basal cells of the remaining JE, which show higher proliferation activity, are involved in JE regeneration. Reduced ODAM expression during proliferation of JE cells may increase again after JE regeneration is complete. Therefore, ODAM may be associated with the normal function of JE.


Key Engineering Materials | 2006

Porous Titanium Membranes Combined with Various Graft Materials Induce Exophytic Bone Formation in Rabbit Calvaria

Yoon Hyuk Kim; Y.H. Kown; Joon-Bong Park; Jong-Hyuk Chung; H.N. Lim; Seong-Suk Jue; M.I. Cho; Yeek Herr

The purpose of this study was to examine if the application of custom-made porous titanium membranes combined with bone graft materials promotes exophytic bone formation in rabbit calvaria. For this purpose, round decorticated calvaria sites were created using a round carbide bur. In the control group, rectangular parallelepiped-shaped porous titanium membranes (RPTMs) were placed on the decorticated sites and fixed with metal pins. In the experimental groups, RPTMs were filled with one of the following bone graft materials prior to fixing with metal pins: bovine bone mineral (BBM), demineralized freeze-dried human cortical bone (DFDB) or freeze-dried human cancellous bone (FDB). Animals were sacrificed at 8 and 12 weeks after surgery, and new bone formation was assessed by histomorphometric as well as statistical analysis. The results indicate that at 8 and 12 weeks, all the experimental groups demonstrated exophytic bone formation. At 12 weeks, DFDB group revealed the most new bone formation (p<0.05) and resorption of grafted materials (p<0.05). On the basis of these findings, we conclude that RPTMs may be used as an augmentation membrane for guided bone regeneration and DFDB as an effective bone-inducing graft material.


The American Journal of Chinese Medicine | 2015

Cudraxanthone H Induces Growth Inhibition and Apoptosis in Oral Cancer Cells via NF-κB and PIN1 Pathways

Hwa-Jeong Lee; Seong-Suk Jue; Soo-Kyung Kang; Won-Jung Bae; Youn-Chul Kim; Eun-Cheol Kim

Cudraxanthone H (CH) is a natural compound isolated from a methanol extract of the root bark of Cudrania tricuspidata, a herbal plant also known as Moraceae. However, the effect of CH on human cancer cells has not been reported previously. The aim of this study was to investigate the anticancer effects and mechanism of action of CH on oral squamous cell carcinoma (OSCC) cells. CH exerted significant antiproliferative effects on OSCC cells in dose- and time-dependent manners. CH also induced apoptosis in OSCC cells, as evidenced by an increased percentage of cells in the sub-G1 phase of the cell cycle, annexin V-positive/propidium iodide-negative cells, and nuclear morphology. This antiproliferative effect of CH was associated with a marked reduction in the expression of cyclin D1 and cyclin E, with a concomitant induction of cyclin-dependent kinase inhibitor (CDKI) expression (p21 and p27). CH inhibited the phosphorylation and degradation of IκB-α and the nuclear translocation of NF-κB p65. Furthermore, CH treatment down-regulated PIN1 mRNA and protein expression in a dose-dependent manner. PIN1 overexpression by infection with adenovirus-PIN1 (Ad-PIN1) attenuated the CH-induced growth-inhibiting and apoptosis-inducing effects, blocked CH-enhanced CDKI expression and restored cyclin levels. In contrast, inhibiting PIN1 expression via juglone exerted the opposite effects. The present study is the first to demonstrate antiproliferative and apoptosis-inducing effects of CH, which exerts its effects by inhibiting NF-κB and PIN1. These data suggest that it might be a novel alternative chemotherapeutic agent for use in the treatment of oral cancer.

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