Ju Yeon Ban

Dankook University, Eidō, Chungcheongbuk-do, South Korea

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Publications (14)17.13 Total impact

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    ABSTRACT: The association between matrix metalloproteinase 2 (MMP2) gene polymorphisms and cancer risk has been investigated in many published studies; however, the currently available results are inconclusive. Therefore, we performed a meta-analysis to provide conclusive evidence for an association between the MMP2 polymorphism (-735 C/T) and cancer risk. Sixteen case-control studies with 11792 individuals were included in this meta-analysis. The odds ratio (OR) and 95% confidence interval (95% CI) were used to investigate the strength of the association. Overall, the MMP2 polymorphism (-735 C/T) was not associated with cancer risk in any of the models. However, the subgroup analysis revealed that dominant model (C/T+T/T vs. C/C: OR=1.24, 95% CI=1.01-1.53) and codominant 1 model (C/T vs. C/C: OR=1.30, 95% CI=1.05-1.62) were significantly associated with cancer risk in the Caucasian population. In conclusion, our meta-analysis indicated that the MMP2 polymorphism (-735 C/T) might be genetic risk factor for the carcinogenesis in Caucasians. However, more studies with a larger sample size are needed to provide more precise evidence.
    No preview · Article · Oct 2015 · International Journal of Clinical and Experimental Medicine
  • Ju Yeon Ban · Sang Wook Kang · Gyeong-Ju Park
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    ABSTRACT: In order to perform successful dental implantations and solve other problems such as bone deficiencies, it is important to find suitable biomaterials to enhance osteoinduction. Heparin has been known to enhance bone morphogenetic protein 2 (BMP-2) induced-bone formation. We histomorphometrically investigated the enhancing effects and roles of heparin to recombinant human bone morphogenetic proteins-2 (rhBMP-2). For morphologic study, stem cells obtained from rabbit adipose tissue were divided into four groups based on heparin concentrations, with a constant rhBMP-2 concentration. They were cultured for 2, 4, and 8 days. Alkaline phosphatase and calcium content were measured as time schedules. In addition, a mixture of rhBMP-2 and heparin was blotted into multiporous anorganic bovine bone and was inserted into calvarial defects in rabbits. The harvested tissues were stained using the Hematoxylin & Eosin (H&E) and Masson's trichrome (MT) stain. And the areas of newly formed bone in the grafted material were analyzed. In morphologic results, the degree of osteoblastic differentiation was significantly increased with increasing heparin concentrations, but the cellular degeneration was accelerated at a higher concentration of heparin as time passed. In histological results, the more higher the concentration of heparin, larger newly formed bone in grafted materials was also observed in the initial period. However, the increased amount of the newly formed bone in grafted materials was progressively decreased at higher concentrations of heparin as time passed. In conclusion, heparin might have an influence on the osteoinductive effects of rhBMP-2 during the initial stage of bone formation.
    No preview · Article · Sep 2015 · Animal cells and systems the official publication of the Zoological Society of Korea
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    ABSTRACT: Periodontitis is one of the most common bacterial and infectious diseases characterized by deepening of the periodontal pockets and loss of attachment, and tooth loss. Periodontitis is associated with high levels of various pro-inflammatory mediators, which result in extensive destruction of connective and bone tissues. The aim of this study was to investigate gene expression profiling related periodontitis in gingival tissues of the ligature induced periodontitis rat model. The periodontitis rat model was induced using ligation of the left and right maxillary second molars during 2 weeks. Micro-computed tomography (CT) was performed to identify bone loss of the teeth. To determine the gene expression profile related to periodontitis, up and down regulated gene expression was analyzed using a cDNA microarray (Affymetrix). Differentially expressed gene (DEG) analysis showed that 40 genes were expressed differentially in gingival tissues of the ligature-induced periodontitis rat model compared to those of normal rats (25 up-regulated genes and 15 down-regulated genes). The DAVID system was carried out to identify functional category and signal pathway. It was found that the regulation of these genes be associated with progress of periodontitis in gingival tissues. Microarray data may be helpful for an investigation of the mechanism in the development of periodontitis. © 2015, The Korean Society of Toxicogenomics and Toxicoproteomics and Springer Science+Business Media Dordrecht.
    No preview · Article · Jun 2015 · Molecular and Cellular Toxicology
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    ABSTRACT: Aims: Heat shock protein 70 (HSP70), one of the major HSPs, has been reported to suppress apoptosis and formation of pathogenic proteins in neurodegenerative disorders. Geranylgeranylacetone (GGA), an anti-ulcer drug, induces HSP70 and thereby protects against cellular damage in various diseases. We investigated the effect of GGA on hydrogen peroxide (H2O2)-induced neurotoxicity in human neuroblastoma SH-SY5Y cells. Main methods: H2O2-induced neuronal toxicity was measured by a CCK-8 assay and Hoechst 33342 staining. We also assessed oxidative stress and apoptosis by measuring reactive oxygen species (ROS) generation with 2′,7′-dichlorofluorescein diacetate (DCFH-DA), caspase-3 activity, and mitogen-activated protein kinase (MAPK) pathway. Key findings: GGA showed a concentration-dependent inhibition on H2O2-induced apoptotic cell death. H2O2-induced induction of HSP70 was enhanced by GGA pretreatment. GGA effectively suppressed the up-regulation of Bax and down-regulation of Bcl-2. GGA also blocked the H2O2-induced phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2). In addition, GGA attenuated H2O2-induced ROS generation and caspase-3 activity. Significance: These results demonstrate that GGA protects SH-SY5Y cells from H2O2-induced apoptosis, at least in part by enhancing HSP70 production. Neuroprotective properties of GGA indicate that this compound may be a potential therapeutic agent for the treatment and prevention of neurodegenerative diseases.
    No preview · Article · Apr 2015 · Life sciences
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    ABSTRACT: Angiotensin-converting enzyme (ACE) is the core enzyme in the renin-angiotensin system (RAS), which catalyzes the production of angiotensin II (Ang II). The aim of this study was to determine whether ACE gene is associated with the development of the periodontal disease. To investigate whether ACE is involved in the development of the periodontal disease, 199 periodontal disease patients and 165 control subjects were studied. The ACE insertion/deletion polymorphism was analyzed using polymerase chain reaction (PCR). SNPStats and SPSS 18.0 were used for the analysis of genetic data. Logistic regression models were performed to determine odds ratio (OR), 95% confidence interval (CI), and P value. Genotypic frequencies of I/I, I/D, and D/D were 25.4%, 42.3%, and 32.3% vs. 35.3%, 41.7%, and 23.1% (periodontal disease group vs. control group), respectively. In the genotype analysis of the ACE insertion/deletion polymorphism, codominant and log-additive models both showed significant association with periodontal disease [OR=1.94, 95% CI=1.05-3.61, P=0.036 in the codominant model (I/I vs. D/D); OR=1.39, 95% CI=1.02-1.90, P=0.034 in the log-additive model (I/I vs. I/D vs. D/D)]. These results suggest that the ACE insertion/deletion polymorphism may be associated with the susceptibility to the periodontal disease in the Korean population. Copyright © 2014 Elsevier Ltd. All rights reserved.
    No preview · Article · Dec 2014 · Archives of Oral Biology
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    Ju Yeon Ban · Koo Han Yoo
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    ABSTRACT: Purpose Benign prostatic hyperplasia (BPH) is the most common prostate disease in aging men. Microseminoprotein-beta (MSMB) is abundant in semen. In this study, we investigated association between single nucleotide polymorphisms (SNPs) at the promoter of the MSMB gene and the risk for developing BPH in a Korean population. Methods We genotyped two promoter polymorphisms (rs12770171, -184C/T and rs10993994, -2C/T) of the MSMB gene by direct sequencing. Ninety-five BPH patients and 78 control subjects were recruited for this study. SNPStats and Haploview version 4.2 were used for genetic analyses. Multiple logistic regression models (codominant, dominant, recessive, and log-additive models) were applied to determine the odds ratio (OR), 95% confidence interval (CI), and P-value. Results Genotype frequency of the rs12770171 SNP showed significant difference between BPH patients and controls (OR, 2.14; 95% CI, 1.07-4.27; P=0.032 in the codominant 1 model; OR, 2.31; 95% CI, 1.19-4.47; P=0.011 in the dominant model; and OR, 2.05; 95% CI, 1.17-3.61; P=0.009 in the log-additive model). Moreover, the SNP also showed association between the two groups (OR, 2.05; 95% CI, 1.19-3.52; P=0.009). The rs10993994 SNP was not associated with BPH. In haplotype analysis, CC and TT haplotypes were associated with BPH (P<0.05). Conclusions This result indicates that a promoter polymorphism (rs12770170, -184C/T) in the MSMB gene may be associated with BPH development in a Korean population.
    Preview · Article · Jun 2014 · International neurourology journal
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    ABSTRACT: To determine whether ACE insertion/deletion (I/D) polymorphism is associated with the ossification of the posterior longitudinal ligament (OPLL) of the spine in the Korean population. A case-control study was conducted to investigate the association between I/D polymorphism of the angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 (ACE) gene and OPLL. The 95 OPLL patients and 274 control subjects were recruited. Polymerase chain reaction for the genotyping of ACE I/D polymorphism was performed. The difference between the OPLL patients and the control subjects was compared using the contingency χ(2) test and the logistic regression analysis. For statistical analysis, SPSS, SNPStats, SNPAnalyzer, and Helixtree programs were used. The genotype and allele frequencies of ACE I/D polymorphism showed significant differences between the OPLL patients and the control subjects (genotype, p<0.001; allele, p=0.009). The frequencies of D/D genotype and D allele in the OPLL group were higher than those in the control group. In logistic regression analysis, ACE I/D polymorphism was associated with OPLL (dominant model; p=0.002; odd ratio, 2.20; 95% confidence interval, 1.33-3.65). These results suggest that the deletion polymorphism of the ACE gene may be a risk factor for the development of OPLL in the Korean population.
    Full-text · Article · Feb 2014 · Annals of Rehabilitation Medicine
  • S.W. KANG · J. CHO · J.Y. BAN · G. CHUN · H. PARK · J.H. CHUNG
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    ABSTRACT: Objectives: Cigarette smoke is a complex mixture of more than 4700 chemical compounds including free radicals and oxidants and it is world widely known problem to health. Nicotine is major compound of tobacco in higher concentrations and known as the cause of gingivitis and periodontitis. It induces intracellular oxidative stress recognized as the important agents involved in the damage of biological molecules. The aim of this study is to clarify the cytotoxic pathway of nicotine in human gingival fibroblasts (HGFs). Methods: Human gingival fibroblast exposed to simulated nicotine was used as an in vitro model. A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was use to detect cell viability and reactive oxygen species (ROS) generation was assessed with DCF-DA. Morphological change was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) Assay, stained with 4,6-diamidino-2-phenylindole (DAPI) stain method. To delineate the roles of ERK, P38 and JNK, western blot and caspase-3 activity assay was performed. Results: Exposure of the human gingival fibroblast to nicotine reduced cell viability by time and dose dependent, increased the generation of ROS, induced morphological evidence of increased apoptosis, resulted in transient activation of JNK and ERK concomitant with activation of P38, and stimulated apoptosis as evidenced by CASP3 activation and PARP cleavage. Conclusion: These results suggest that nicotine induces apoptosis through the ROS generation and caspase-3 dependent pathways in HGFs.
    No preview · Conference Paper · Mar 2011
  • J. BAN · S.W. KANG · C. LEE · J. CHO
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    ABSTRACT: Objectives: The present study was performed to evaluate the associations of collagen, type VI, alpha 2 (COL6A2) polymorphisms with oral squamous cell carcinoma risks in Korean population. Methods: We recruited oral squamous cell carcinoma patients and healthy individuals, and genotyped the locus of COL6A2 polymorphisms (rs1475915; promoter, rs914244; promoter, rs1042917; missense, and rs914244; missense) by combining the polymerase chain reaction-restriction fragment length polymorphism method and direct sequencing. Results: Genotype distributions of the rs1475915 polymorphism showed significant association between the oral squamous cell carcinoma and the control groups (P<0.001). And, other polymorphisms did not show any significant association between oral squamous cell carcinoma and control. Conclusion: This result suggests that COL6A2 polymorphism may be associated with oral squamous cell carcinoma in Korean population.
    No preview · Conference Paper · Jul 2010
  • S.W. KANG · J. BAN · J. CHO
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    ABSTRACT: Objectives: High invasiveness and anti-apoptotic feature of oral squamous cell carcinoma (OSCC) is important for the prognosis of cancer. Dysregulation of apoptosis increases aberrant cells and the probability of mutation that might lead to carcinogenesis. Angiogenesis is deeply associated with high invasiveness and invasion of tumor makes a poor prognosis and survival rate. SIVA1 plays an important role in the apoptosis signaling pathway in various cells. Recent studies showed SIVA1 regulates apoptosis in cancer cells via some pathways. And some authors reported ALOX5 is overexpressed in cancer cells and promotes cancer cell growth and neo-angiogenesis. Also, aberrant expression of ALOX5AP has a relation with cancers, especially in aggressive tumours. The aim of this study was to identify the hypothesis that single nucleotide polymorphism (SNP) in SIVA1, ALOX5, and ALOX5AP correlates with oral squamous cell carcinoma in a Korean population. Methods: We investigated the distribution of genotypes and alleles in SIVA1, ALOX5, and ALOX5AP genes in patients with OSCC and age- and gender matched controls. Genomic DNA was extracted from paraffin embedded tissue. A total of four single nucleotide polymorphisms on the SIVA1, ALOX5, and ALOX5AP genes were selected [SIVA1 (rs1132975, synonymous), ALOX5 (rs2228064, synonymous), and ALOX5AP (rs17222919 and rs312466, promoter)]. The genotypes were determined using direct sequencing and analyzed with SNPStats and SPSS 17.0. Results: The genotype distributions of rs1132975 SNP of SIVA1 and rs17222814 SNP of ALOX5AP genes showed significant difference between controls and OSCC (p<0.001, respectively). Conclusions: This result suggests that polymorphisms of SIVA1 and ALOX5AP may be associated with OSCC in Korean population.
    No preview · Conference Paper · Jul 2010

  • No preview · Article · Sep 2008 · International Journal of Psychophysiology

  • No preview · Article · Sep 2008 · International Journal of Psychophysiology

  • No preview · Article · Sep 2008 · International Journal of Psychophysiology
  • S.W. KANG · H.J. PARK · J.H. CHUNG · J.O. CHO · J.Y. BAN
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    ABSTRACT: Objectives: Cigarette smoke is a complex mixture of more than 4700 chemical compounds including free radicals and oxidants and it is worldwide problem to health. Nicotine is major compound of tobacco in higher concentrations and it induces intracellular oxidative stress recognized as the important agents involved in the damage of biological molecules. The aim of this study is to clarify the effect of nicotine to human gingival fibroblast. Methods: Human gingival fibroblast exposed to simulated nicotine was used as an in vitro model. The 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) assay was use to detect cell viability and ROS generation was assessed with 2,7-dichlorofluoroscein diacetate (DCF-DA). Morphological change was detected by Terminal Deoxynucleotidyl Transferase-mediated dUTP Nick End Labeling (TUNEL) Assay, staining with 3,3'-diaminobenzidine (DAB) and 4,6-Diamidino-2-Phenylindole (DAPI) Staining. To delineate the role(s) of extracellular signal-regulated kinase (ERK), p38 and c-Jun NH2-terminal protein kinase (JNK), western blot and caspase-3 (CASP3) activity assay was performed. Results: Exposure of the HGF to nicotine reduced cell viability by time and dose dependent, increased the generation of ROS, induced morphological evidence of increased apoptosis, resulted in transient activation of JNK and ERK concomitant with activation of p38, and stimulated apoptosis as evidenced by CASP3 activation and poly(ADP-ribose) polymerase (PARP) cleavage. Conclusion: Our results suggest that nicotine induces apoptosis through caspase-3 activation in human gingival fibroblast.
    No preview · Conference Paper ·