Hyoung-Chin Kim

Korea Research Institute of Bioscience and Biotechnology KRIBB, Anzan, Gyeonggi Province, South Korea

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Publications (54)151.73 Total impact

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    ABSTRACT: This study investigated the time-course of 1,3-dichloro-2-propanol (1,3-DCP)-induced hepatotoxicity and the molecular mechanism of its oxidative stress and apoptotic changes in rats. Thirty-six male rats were randomly assigned to six groups of six rats each and were administered a single oral dose of 1,3-DCP (90mg/kg) or its vehicle. 1,3-DCP caused acute hepatic damage, as evidenced by marked increases in serum aminotransferase, alkaline phosphatase, and histopathological alterations. These functional and histopathological changes in the liver peaked at 12h after administration and then decreased progressively. Oxidative stress indices were increased significantly at 6h, peaked at 12h, and then decreased progressively. The number of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)- and caspase-3-positive cells increased after 6h, peaked at 12 and 24h, and then decreased. The protein levels of phosphorylated mitogen-activated protein kinases (MAPKs) including p-Erk1/2 and p-JNK showed a similar trend to the numbers of TUNEL- and caspase-3-positive cells. These results indicate that 1,3-DCP increases oxidative stress, nuclear translocation of Nrf2, and expression of Nrf2-targeted genes, followed by increased functional and histopathological alterations in the liver. The increase in hepatocellular apoptosis induced by 1,3-DCP may be related to oxidative stress-mediated MAPK activation. Copyright © 2015 Elsevier B.V. All rights reserved.
    06/2015; 40(1). DOI:10.1016/j.etap.2015.06.011
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    ABSTRACT: A novel Helicobacter species was identified from the gastrointestinal tract of Korean striped field mice (Apodemus agrarius). Biochemical testing, ultrastructure characterization, and 16S rRNA gene sequence analysis suggested that this bacterium represents a distinct taxon. The bacterium was positive for urease activity, susceptible to cephalothin and nalidixic acid, and weakly positive for oxidase and catalase activity. Electron microscopy revealed that the bacterium has spirally curved rod morphology with singular bipolar nonsheathed flagella. Genotypically, the isolated bacterial strains (YMRC 000215, YMRC 000216, and YMRC 000419) were most closely related to a reference strain of Helicobacter mesocricetorum (97.25%, 97.32%, and 97.03% 16S rRNA sequence similarities, respectively). The 16S rRNA sequences of these strains were deposited into GenBank under accession numbers AF284754, AY009129, and AY009130, respectively. We propose the name Helicobacter apodemus for this novel species.
    Journal of veterinary science (Suwŏn-si, Korea) 03/2015; · 1.14 Impact Factor
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    ABSTRACT: The leptin receptor-deficient db/db mouse is a rodent model of type 2 diabetes and obesity. Diabetes in db/db mice shows an age-dependent progression, with early insulin resistance followed by an insulin secretory defect resulting in profound hyperglycemia. However, there is insufficient data on agedependent changes of energy metabolism in db/db mice. We demonstrated an age-dependent decrease in the respiratory exchange ratio (RER), calculated by a ratio of VO2/VCO2, in db/db mice. The RER determined by indirect calorimetry, was 1.03 in db/db mice under 6 weeks of age, which were similar to those in heterozygote (db/+) and wild-type (+/+) mice. However, RER decreased from approximately 0.9 to 0.8 by 10 weeks of age and subsequently returned to approximately 0.9 at 22 weeks of age. The changes in RER were concurrent with the alterations in body weight and blood glucose level. However, other metabolic indicators such as glucose tolerance, changes in body fat mass, and urinary glucose levels, did not change with age. The results suggested that the energy source utilized in db/db mice changed with the age-related progression of diabetes.
    03/2015; 31(1):1-6. DOI:10.5625/lar.2015.31.1.1
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    ABSTRACT: Background & Aims: Non-alcoholic fatty liver disease (NAFLD) is strongly associated with obesity and type 2 diabetes. Thioredoxin-interacting protein (TXNIP) regulates the cellular redox state and metabolism and has been linked to many diseases, including diabetes. Therefore, we examined the role of TXNIP in hepatic steatosis in vitro and in vivo. Methods: Lipogenic and inflammatory proteins produced by hepatocytes treated with palmitic acid (PA) or transfected with TXNIP or Txnip siRNA were measured by Western blotting. Lipid accumulation was assessed using Oil Red 0 staining. Protein interactions were assessed by immunoprecipitation and proximity ligation assay. Hepatic protein levels were measured by Western blotting from wild type or Txnip(-/-) mice fed a high-fat diet (HFD) or chow diet. Livers from NAFLD patients were compared with normal liver by immunohistochemistry. Results: PA increased TXNIP, and inflammatory and lipogenic proteins in both AML12 and H4IIE cells. It also increased the peroxisome proliferator-activated receptor gamma co-activator-1 alpha (PGC-1 alpha), which mediated the expression of lipogenic markers and lipid accumulation. In addition, PA increased protein arginine methyltransferase-1 (PRMT1) and PRMT1 siRNA abolished the increase in lipogenic markers with PGC-1 alpha. Furthermore, TXNIP interacted with PRMTI in PA-treated hepatocytes. In vivo, levels of lipogenic proteins, inflammatory molecules, PGC-1 alpha, and PRMT1 were increased in the livers of HFD mice compared with those fed a chow diet, and were ameliorated in HFD Txnip(-/-) mice. Moreover, TXNIP, PRMT1, and PGC-1 alpha were elevated in the livers of human NAFLD patients. Conclusions: TXNIP mediates hepatic lipogenesis via PRMT1 and PGC-1 alpha regulation and inflammation in vitro and in vivo, implying that targeting TXNIP and PRMT1 is a potential therapeutic approach for treatment of NAFLD.
    Journal of Hepatology 07/2014; 61(5). DOI:10.1016/j.jhep.2014.06.032 · 10.40 Impact Factor
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    ABSTRACT: We investigated the protective effects of pine bark extract (Pycnogenol®, PYC, Horphag Research Ltd., Route de Belis, France) against α-chlorohydrin (ACH)-induced spermatotoxicity in rats. Rats were orally administered ACH (30 mg/kg/day) with or without PYC (20 mg/kg/day) for 7 days. Administration of ACH significantly decreased sperm motility. α-Chlorohydrin also caused histopathological alterations and apoptotic changes in caput epididymides. An increased malondialdehyde concentration and decreased glutathione content, as well as catalase and glutathione peroxidase activities were also found. In contrast, PYC treatment significantly prevented ACH-induced spermatotoxicity, including decreased sperm motility, histopathological lesions, and apoptotic changes in the caput epididymis. Pycnogenol® also had an antioxidant benefit by decreasing malondialdehyde and increasing levels of the antioxidant glutathione and the activities of the antioxidant enzymes catalase and peroxidase in epididymal tissues. These results indicate that PYC treatment attenuated ACH-induced spermatotoxicity through antioxidant and antiapoptotic effects. © 2013 The Authors. Phytotherapy Research published by JohnWiley & Sons, Ltd.
    Phytotherapy Research 03/2014; DOI:10.1002/ptr.5016 · 2.40 Impact Factor
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    ABSTRACT: This study investigated the protective effects of diallyl disulfide (DADS) against cyclophosphamide (CP)-induced acute urotoxicity in rats. CP caused severe hemorrhagic cystitis as shown by significant increases in bladder weight, edema, and hemorrhage as well as increased urinary bladder epithelial cell apoptosis, protein expression of nuclear factor erythroid 2-related factor-2 (Nrf-2) and phase II enzymes (i.e. quinine oxidoreductase-1 (NQO-1) and heme oxygenase-1 (HO-1)), immunostaining intensity of acrolein-protein adducts, and histopathological changes. The significant decreases in glutathione content and catalase, glutathione-S-transferase, and glutathione reductase activities and a significant increase in malondialdehyde content indicated that CP-induced bladder injury was mediated through oxidative stress. In contrast, pretreatment with DADS significantly attenuated the CP-induced urotoxic effects, including oxidative damage, histopathological lesions, apoptotic changes, and accumulation of acrolein-protein adducts in the bladder. DADS also significantly increased expression of CYP2B1/2, CYP3A1, Nrf-2, NQO-1, and HO-1 and significantly decreased expression of CYP2C11. These results indicate that DADS prevented CP-induced bladder toxicity, in part, by detoxifying acrolein. The protective effects of DADS may be due to its ability to decrease metabolic activation of CP by inhibiting CYP2C11 and inducing CYP3A1, and its potent antioxidant activity and antiapoptotic effects occurred via the Nrf-2-antioxidant response element pathway.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 11/2013; 64. DOI:10.1016/j.fct.2013.11.023 · 2.61 Impact Factor
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    ABSTRACT: This study was conducted to investigate the potential effects of diallyl disulfide (DADS) on carbon tetrachloride (CCl4 )-induced acute hepatotoxicity and to determine the molecular mechanisms of protection offered by DADS in rats. DADS was administered orally at 50 and 100 mg/kg/day once daily for 5 consecutive days prior to CCl4 administration. The single oral dose of CCl4 (2 mL/kg) caused a significant elevation in serum aspartate and alanine aminotransferase activities, which decreased upon pretreatment with DADS. Histopathological examinations showed extensive liver injury, characterized by extensive hepatocellular degeneration/necrosis, fatty changes, inflammatory cell infiltration, and congestion, which were reversed following pretreatment with DADS. The effects of DADS on cytochrome P450 2E1 (CYP2E1), the major isozyme involved in CCl4 bioactivation, were also investigated. DADS pretreatment resulted in a significant decrease in CYP2E1 protein levels in dose-dependent manner. In addition, CCl4 caused a decrease in protein level of cytoplasmic nuclear factor E2-related factor 2 (Nrf2) and suppression of nuclear translocation of Nrf2 concurrent with downregulation of detoxifying phase II enzymes and a decrease in antioxidant enzyme activities. In contrast, DADS prevented the depletion of cytoplasmic Nrf2 and enhanced nuclear translocation of Nrf2, which, in turn, upregulated antioxidant and/or phase II enzymes. These results indicate that the protective effects of DADS against CCl4 -induced hepatotoxicity possibly involve mechanisms related to its ability to induce antioxidant or detoxifying enzymes by activating Nrf2 and block metabolic activation of CCl4 by suppressing CYP2E1. © 2013 Wiley Periodicals, Inc. Environ Toxicol, 2013.
    Environmental Toxicology 11/2013; 30(5). DOI:10.1002/tox.21930 · 3.23 Impact Factor
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    ABSTRACT: The present study investigated the possible ameliorative effects of melatonin (MLT) against adriamycin (ADR)-induced hepatotoxicity and oxidative stress in rats. The following four experimental groups were evaluated: (1) vehicle control, (2) MLT (15 mg/kg/day), (3) ADR (10 mg/kg), and (4) ADR&MLT. ADR caused severe hepatotoxicity as evidenced by an elevation of serum aspartate aminotransferase and alanine aminotransferase activities, increased total bilirubin concentration, and decreased albumin and total protein concentration, indicating hepatic function abnormalities. Histopathological examination revealed various structural changes in liver, characterized by hepatocyte degeneration/necrosis, congestion, sinusoidal dilatation, vacuolation, and inflammatory cell infiltration. The significant decrease in reduced glutathione (GSH) content, catalase, superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione reductase (GR) activities and the significant increase in malondialdehyde (MDA) content indicated that ADR-induced hepatotoxicity was mediated through oxidative stress. In contrast, MLT treatment significantly improved ADR-induced serum biochemical and histo-pathological alterations reflecting hepatic dysfunction. Moreover, MDA concentration and GSH content, GR, GPx, and SOD activities were not affected when MLT was administered in conjunction with ADR. These results indicated that MLT improved the oxidative damage induced by ADR in rat liver, presumably due to its ability to inhibit lipid peroxidation, and restore both enzymatic and nonenzymatic antioxidant activities.
    Molecular and Cellular Toxicology 09/2013; 9(3):257-265. DOI:10.1007/s13273-013-0033-0 · 0.83 Impact Factor
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    ABSTRACT: Reactive oxygen species (ROS) are critical determinants of the fate of hematopoietic stem cells (HSCs) and hematopoiesis. Thioredoxin-interacting protein (TXNIP), which is induced by oxidative stress, is a known regulator of intracellular ROS. Txnip(-/-) old mice exhibited elevated ROS levels in hematopoietic cells and showed a reduction in hematopoietic cell population. Loss of TXNIP led to a dramatic reduction of mouse survival under oxidative stress. TXNIP directly regulated p53 protein by interfering with p53- mouse double minute 2 (MDM2) interactions and increasing p53 transcriptional activity. Txnip(-/-) mice showed downregulation of the antioxidant genes induced by p53. Introduction of TXNIP or p53 into Txnip(-/-) bone marrow cells rescued the HSC frequency and greatly increased survival in mice following oxidative stress. Overall, these data indicate that TXNIP is a regulator of p53 and plays a pivotal role in the maintenance of the hematopoietic cells by regulating intracellular ROS during oxidative stress.
    Cell metabolism 07/2013; 18(1):75-85. DOI:10.1016/j.cmet.2013.06.002 · 16.75 Impact Factor
  • 06/2013; 14(2):111-117. DOI:10.12729/jbr.2013.14.2.111
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    ABSTRACT: Deregulated Wnt signaling pathway is implicated in many hereditary diseases and tumorigenesis including colorectal cancer, hepatocellular carcinoma and gastric cancer. In this study, to assess the relationship between chemically induced gastric tumor and canonical Wnt signaling pathway in genetically intact mice, histopathological and quantitative mRNA analyses were performed in C57BL/6J mice given drinking water containing N-methyl-N-nitrosurea (MNU). 60.5% of gastric adenoma and 27.9% of adenocarcinoma were observed 48 weeks after first administration. Also, in immunohistochemical analysis, aberrant expressions of phospho-GSK-3β, β-catenin, cyclin D1, c-Myc, osteopontin and COX-2 were found. In double immunofluorescent-antibody stains, β-catenin accumulation was colocalized with other proteins. mRNA levels of cyclin D1, c-myc and COX-2 were relatively higher in adenocarcinoma. Altogether, canonical Wnt pathway was highly involved in MNU induced gastric neoplasia of C57BL/6J mice, and it could be a considerably suitable system for the study to examine the linkage between gastric tumorigenesis and the canonical Wnt pathway.
    Journal of Veterinary Medical Science 10/2012; 75(3). DOI:10.1292/jvms.12-0233 · 0.88 Impact Factor
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    09/2012; 13(3):229-235. DOI:10.12729/jbr.2012.13.3.229
  • Sang Yoon Lee · Ji-Yoon Lee · Soo Jin Oh · Hyoung-Chin Kim · Sang Kyum Kim
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    ABSTRACT: The regulation of antioxidant enzymes has received increased attention in terms of protection from many diseases. Despite reports that administered estradiol derivatives can change antioxidant enzyme levels, comprehensive information is not available regarding the effects of the human menstrual cycle or the rat estrous cycle on the expression of the antioxidant enzyme system. The present study was performed to determine the expression levels of cytosolic antioxidant enzymes, including superoxide dismutase-1, catalase, glutathione peroxidase-1, glutathione reductase, peroxiredoxin (Prx)-1, Prx-2, thioredoxin-1, gamma-glutamylcysteine ligase catalytic subunit, alpha-class glutathione S-transferase (GST), pi-class GST, and mu-class GST, in the liver and ovaries of female rats during diestrus and proestrus. Our results indicate that hepatic expression of Prx-1 and Prx-2, and ovarian expression of alpha-class GST were increased significantly during the proestrus phase compared with the diestrus phase. These results suggest that the hepatic Prx family and ovarian alpha-class GST are sensitive to changes during the estrous cycle. Further studies are needed to determine the physiological significance of the regulation of the Prx family and alpha-class GST during the estrous cycle.
    Toxicology Letters 06/2012; 212(3):329-36. DOI:10.1016/j.toxlet.2012.06.006 · 3.36 Impact Factor
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    ABSTRACT: The present study investigated the protective effects of melatonin (MT) against gentamicin (GM)-induced nephrotoxicity and oxidative stress in rats. We also investigated the effects of MT on induction of apoptotic cell death and its potential mechanisms in renal tissues in response to GM treatment. The following four experimental groups were evaluated: (1) vehicle control, (2) MT (15 mg/kg/day), (3) GM (100 mg/kg/day), and (4) GM&MT. GM caused severe nephrotoxicity as evidenced by increased serum blood urea nitrogen and creatinine levels, increased renal tubular cell apoptosis, and increased Bcl2-associated X protein and cleaved caspase-3 protein expression. Additionally, GM treatment caused an increase in levels of inducible nitric oxide synthase (iNOS) and nuclear factor-kappa B (NF-κB) protein expression in renal tissues. The significant decreases in glutathione content, catalase, superoxide dismutase, glutathione-S-transferase, glutathione peroxidase, and glutathione reductase activities and the increase in malondialdehyde content indicated that GM-induced tissue injury was mediated through oxidative reactions. In contrast, MT treatment protected kidney tissue against the oxidative damage and the nephrotoxic effect caused by the GM treatment. Histopathological studies confirmed the renoprotective effect of MT. These results indicate that MT prevents nephrotoxicity induced by GM in rats, presumably because it is a potent antioxidant, restores antioxidant enzyme activity, and blocks NF-κB and iNOS activation in rat kidney.
    Archives of Toxicology 04/2012; 86(10):1527-36. DOI:10.1007/s00204-012-0849-8 · 5.08 Impact Factor
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    ABSTRACT: This study was conducted to investigate the potential effects of α-chlorohydrin (ACH) on epididymal function and antioxidant system in male rats. The test chemical was administered to male rats by gavage at doses of 0, 3, 10, and 30 mg/kg/day for 7 days. Twenty-four male rats were randomly assigned to four experimental groups, with six rats in each group. Spermatotoxicity was assessed by measurement of reproductive organ weight, testicular sperm head count, epididymal sperm motility and morphology, histopathologic examination, and oxidative damage analysis in rats. At 30 mg/kg/day, an increase in the incidence of clinical signs, epididymis weight, and gross necropsy findings of the epididymis, a decrease in the sperm motility, and an increased incidence of histopathological changes of the epididymis were observed in a dose-dependent manner. At 10 mg/kg/day, an increased incidence of clinical signs and histopathological changes and decreased sperm motility were observed. In the oxidative damage analysis, an increase in the malondialdehyde concentration and a decrease in the glutathione content and glutathione peroxidase and catalase activities in the epididymal tissue were detected at ≥3 mg/kg/day. The results show that graded doses of ACH elicit depletion of the antioxidant defense system and that the spermatotoxicity of ACH may be due to the induction of oxidative stress.
    03/2012; 28(1):11-6. DOI:10.5625/lar.2012.28.1.11
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    ABSTRACT: In this study, we investigated the effect of methanolic extract isolated from the root of Lycoris aurea (LA) on the growth of cancer cells and the tube formation activity of endothelial cells. Various cancer cells were treated with LA at doses of 0.3, 1, 3, 10 or 30 μg/ml and LA significantly suppressed the growth of several cancer cell lines, including ACHN, HCT-15, K-562, MCF-7, PC-3 and SK-OV-3, in a dose-dependent manner. We also found that LA induced cell cycle arrest at G2/M phase in ACHN renal cell adenocarcinoma cells. Further study demonstrated that LA concentration-dependently inhibited the tube formation, which is a widely used in vitro model of reorganization stage of angiogenesis, in human umbilical vein endothelial cells. Collectively, these results show that LA inhibits the growth of cancer cells and tube formation of endothelial cells and the growth-inhibitory effect of LA might be mediated, at least in part, by blocking cell cycle progression.
    Toxicological Research 03/2012; 28(1):33-38. DOI:10.5487/TR.2012.28.1.033
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    ABSTRACT: The present study investigated the protective effects of pine bark extract (PBE) against hexavalent chromium [Cr(VI)]-induced dermatotoxicity in rats. Skin reactions were evaluated by visual inspection, histopathological changes and oxidative stress parameters. Topical application of Cr(VI) produced a significant increase in the incidence and severity of erythema and edema upon visual inspection. Histopathological examination showed moderate to severe necrosis and desquamation in the epidermis and inflammation and hemorrhage in the dermis. In addition, an increased malondialdehyde (MDA) concentration, and decreased glutathione (GSH), catalase, superoxide dismutase, glutathione-S-transferase (GST) and glutathione reductase of the skin were observed in the Cr(VI) group. On the contrary, concomitant administration with PBE significantly improved Cr(VI)-induced dermatotoxicity, evidenced by a decrease in the incidence and severity of skin irritation and histopathological lesions in a dose-dependent manner. Moreover, PBE treatment reduced MDA concentrations and increased catalase and GST activities in skin tissues, indicating that concomitant administration with PBE effectively prevents Cr(VI)-induced oxidative damage in rats. The results indicate that PBE has a protective effect against Cr(VI)-induced dermatotoxicity and is useful as a protective agent against various dermal lesions induced by oxidative stress. Copyright © 2012 John Wiley & Sons, Ltd.
    Phytotherapy Research 02/2012; 26(10):1534-40. DOI:10.1002/ptr.4610 · 2.40 Impact Factor
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    ABSTRACT: This study investigated the protective effects of pine bark extract (Pycnogenol®, PYC) against cyclophosphamide (CP)-induced developmental toxicity in rats. A total of 44 mated females were randomly assigned to the following four experimental groups: (1) vehicle control, (2) CP, (3) CP&PYC, or (4) PYC. All dams were subjected to a Caesarean section on day 20 of gestation, and fetuses were examined for morphological abnormalities. Oxidative stress analysis was performed on maternal hepatic tissues. CP treatment caused decreased fetal and placental weights and increased embryonic resorptions and fetal malformations. In addition, an increased malondialdehyde (MDA) concentration and decreased reduced glutathione (GSH) content and catalase activity were observed in the hepatic tissues. On the contrary, PYC treatment during pregnancy significantly ameliorated the CP-induced embryo-fetal developmental toxicity in rats. Moreover, MDA and GSH concentrations and catalase activity in hepatic tissues were not affected when PYC was administered in conjunction with CP. These results suggest that repeated administration of PYC has beneficial effects against CP-induced embryo-fetal developmental toxicity in rats, and that the protective effects of PYC may be due to both inhibition of lipid peroxidation and increased antioxidant activity.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 02/2012; 50(2):109-15. DOI:10.1016/j.fct.2011.10.048 · 2.61 Impact Factor
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    ABSTRACT: Vitamin D(3) upregulated protein 1 (VDUP1) is a potent tumour suppressor whose expression is dramatically reduced in various types of human cancers, including gastric cancer. However, the precise mechanisms underlying tumour development remain unclear. In the present study, the authors examined the effect of VDUP1 on Helicobacter pylori-induced gastric carcinogenesis in mice. Gastric cancer was generated in VDUP1 knockout (KO) and wild-type mice using a combination of N-methyl-N-nitrosourea treatment and H pylori infection. Fifty weeks after treatment, gastric tissues from both types of mice were examined by histopathology, immunohistochemistry and immunoblotting. In vitro tests on the human gastric cancer cell line, AGS, were also performed to identify the underlying mechanisms of cancer development. The overall incidence of gastric cancer was significantly higher in VDUP1 KO mice than in wild-type mice. Similarly, VDUP1 KO mice showed more severe chronic gastritis, glandular atrophy, foveolar hyperplasia, metaplasia and dysplasia. Although no differences in the apoptotic index were apparent, lack of VDUP1 increased the rate of gastric epithelial cell proliferation in non-cancerous stomachs, with corresponding increases in tumour necrosis factor alpha (TNFα) level, nuclear transcription factor kappa B (NF-κB) activation and cyclooxygenase-2 (COX-2) expression. An in vitro study showed that H pylori-associated cell proliferation and induction of TNFα, NF-κB and COX-2 were inhibited in cells transfected with VDUP1. In addition, overexpression of VDUP1 in AGS cells suppressed TNFα-induced NF-κB activation and COX-2 expression. Our data show that VDUP1 negatively regulates H pylori-associated gastric carcinogenesis, in part by disrupting cell growth and inhibiting the induction of TNFα, NF-κB and COX-2. These findings provide important insights into the role of VDUP1 in H pylori-associated tumourigenesis.
    Gut 09/2011; 61(1):53-63. DOI:10.1136/gutjnl-2011-300361 · 13.32 Impact Factor

Publication Stats

500 Citations
151.73 Total Impact Points

Institutions

  • 2003–2014
    • Korea Research Institute of Bioscience and Biotechnology KRIBB
      • • Natural Medicine Research Center
      • • Bio-Evaluation Center
      • • National Research Laboratory of Lipid Metabolism and Atherosclerosis
      Anzan, Gyeonggi Province, South Korea
    • Seoul National University
      Sŏul, Seoul, South Korea
  • 2007
    • Konkuk University
      • Department of Laboratory Medicine
      Sŏul, Seoul, South Korea
  • 2006
    • Hanyang University
      Sŏul, Seoul, South Korea