• Molecular & Cellular Toxicology
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• v.1 no.4
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• pp.224-229
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• 2005

Cirsii Japonici Herba (CJH) extract has been used for hundreds of years in Asian countries as a treatment for pollutant, radiation, and alcohol-induced liver damage. The reducing effect of CJH on hydrogen peroxide-induced reactive oxygen species (ROS) production, the main cause of cell damage or death, was evaluated using the HepG2 cell line. Cell survival was determined using MTS assay. The viability of cells treated with CJH was not significantly different from oxidative-stressed HepG2 cells. A dose-dependent inhibitory effect by CJH on ROS production was shown in oxidative-stressed cells using the $H_{2}DCFDA$ assay. To identify candidate genes responsible for the anti-oxidative effects of CJH on HepG2 cells, an oligonucleotide microarray analysis was performed. The expressions of five genes were decreased, whereas nineteen genes were up-regulated in CJH plus hydrogen peroxide treated cells, compared to only hydrogen peroxide treated cells. Among them, the expression of 5 genes was decreased in hydrogen peroxide treatment when compared to control. These genes are known to regulate cell survival and progression. On the other hand, it was shown that its main compounds were not a sylimarin or its analogs. The list of differentially expressed genes may provide further insight on the action and mechanism behind the anti-oxidative effects of Cirsii Japonici Herba.

• Journal of Crop Science and Biotechnology
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• v.10 no.1
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• pp.50-56
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• 2007

Barley S-adenosylmethionine synthetase1 gene, which was differentially expressed in seed development of extra early barley, was regulated by the phytohormones and abiotic stresses. In order to identify the regulation regions which were involved in transcriptional control of the phytohormones and abiotic stresses, we isolated 1459 bp fragment of HvSAMS1 gene promoter using genome walking strategy and deletion series were constructed. Deleted upstream fragments(-1459, -1223, -999, -766, -545, -301 bp) were fused to the GUS reporter gene and evaluated via Agrobacterium-mediated transient expression assay. Increased GUS activity of HvSMAS1 promoter -301/GUS construct under each of NaCl, $GA_3$, ABA and ethylene application was found. However, GUS activity was negligible in the leaves transformed with the HvSMAS1 promoter(-1459, -1223, -999, -766 and -545)/GUS constructs. No significant induction of GUS activity was observed for the ethionine and spermidine treatments. In order to locate promoter sequence of the HvSAMS1 gene that was critical for the activation of gene expression, deletion and addition promoter derivatives(+, includes 43 bp of 5' ORF) of the HvSAMS1 gene fused to the GUS reporter gene were applied. The tobacco leaves which harbored the additional HvSAMS1 promoter(-1459+, -1459 to -546, -545+ and -301+)/GUS construct did not significantly induce GUS activity as compared to the HvSAMS1 promoter(-1459, -545 and -301)/GUS constructs under each of NaCl, ABA and $GA_3$ treatment. However, the GUS activity was high in the tobacco leaves which harboring the -211 to -141 regions of the HvSAMS1 promoter. This result suggested that HvSAMS1 gene expression might be regulated by this region(from -211 to -141).

• Asian-Australasian Journal of Animal Sciences
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• v.30 no.7
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• pp.1037-1047
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• 2017

Objective: Despite an increasing number of investigations into the pathophysiology of necrotic enteritis (NE) disease, etiology of NE-associated diseases, and gene expression profiling of NE-affected tissues, the microRNA (miRNA) profiles of NE-affected poultry have been poorly studied. The aim of this study was to induce NE disease in the genetically disparate Fayoumi chicken lines, and to perform non-coding RNA sequencing in the intestinal mucosal layer. Methods: NE disease was induced in the Fayoumi chicken lines (M5.1 and M15.2), and non-coding RNA sequencing was performed in the intestinal mucosal layer of both NE-affected and uninfected chickens to examine the differential expression of miRNAs. Next, quantitative real-time polymerase chain reaction (real-time qPCR) was performed to further examine four miRNAs that showed the highest fold differences. Finally, bioinformatics analyses were performed to examine the four miRNAs target genes involvement in the signaling pathways, and to examine their interaction. Results: According to non-coding RNA sequencing, total 50 upregulated miRNAs and 26 downregulated miRNAs were detected in the NE-induced M5.1 chickens. While 32 upregulated miRNAs and 11 downregulated miRNAs were detected in the NE-induced M15.2 chickens. Results of real-time qPCR analysis on the four miRNAs (gga-miR-9-5p, gga-miR-20b-5p, ggamiR-196-5p, and gga-let-7d) were mostly correlated with the results of RNAseq. Overall, ggamiR-20b-5p was significantly downregulated in the NE-induced M5.1 chickens and this was associated with the upregulation of its top-ranking target gene, mitogen-activated protein kinase, kinase 2. Further bioinformatics analyses revealed that 45 of the gene targets of gga-miR-20b-5p were involved in signal transduction and immune system-related pathways, and 35 of these targets were predicted to interact with each other. Conclusion: Our study is a novel report of miRNA expression in Fayoumi chickens, and could be very useful in understanding the role of differentially expressed miRNAs in a NE disease model.

• Journal of Life Science
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• v.17 no.7 s.87
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• pp.996-1001
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• 2007

To investigate whether sulindac, sulindac sulfone, and sulindac sulfide could affect cancer cell viabilities, human colorectal HCTl16 cells were treated with 10 ${\mu}M$ of each NSAID. Among treated NSAms, sulindac sulfide dramatically decreased the cell viabilities detected by MTS and the cytotoxic effect showed dose-dependent manner. To understand the molecular mechanism of cell death in response to sulindac sulfide treatment, we performed oligo DNA microarray analysis. We found that 23 genes were up-regulated more than 2 folds, whereas 33 genes were down-regulated more than 2 folds by treatment of 10 ${\mu}M$ sulindac sulfide. Among the up-regulated genes, we selected 3 genes (NAG-1, DDIT3, PCK2) and performed RT-PCR and quantitative real-time PCR to cofirm microarray data. The results of RT-PCR and real-time PCR were highly accorded with those of microarray experiment. As NAG-1 is well-known gene as tumor suppressor, we detected changes of NAG-1 expression by 10 ${\mu}M$ of sulindac, sulindac sulfone, and sulindac sulfide. The results of RT-PCR and quantitacve real-time PCR indicated that sulindac sulfide was the strongest inducer of NAG-1 among treated NSAIDS. This result implies that induction of NAG-1 by sulindac sulfide plays important role in cell death of colorectal cancer. Overall, we speculate that these results may be helpful in understanding the molecular mechanism of the cancer chemoprevention by sulindac sulfide in human colorectal cancer.

• Journal of Life Science
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• v.22 no.11
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• pp.1523-1528
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• 2012

In a previous proteomic study, heat shock protein beta 1 (HSPB1) was detected as differentially expressed protein in longissimus thoracis between low (grade 3) and high (grade 1++) meat quality groups by 2DE gel electrophoresis. The present study investigated an association of HSPB1 expression at the level of gene and protein with Warner-Bratzler shear force (WBS) measured in 20 Hanwoo steers. An analysis of variance (ANOVA) between expression values and WBS showed that WBS was affected by HSPB1 expression (p<0.05). The expression (at both gene and protein level) of the HSPB1 was 2 times higher in the low WBS group than that in the high WBS group (p<0.01). This result suggests that the HSPB1 gene may be a candidate gene associated with tenderness in longissimus thoracis of Korean cattle.

• Microbiology and Biotechnology Letters
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• v.38 no.4
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• pp.442-447
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• 2010

We investigated anti-cancer and anti-proliferative activity of allicin and analyzed global gene expression changes by allicin treatment in human colorectal HCT116 cells. As a result, allicin decreased cell viabilities in a dose and time-dependent manner and induced apoptosis. Oligo DNA microarray analysis, we found that 7,840 genes were up-regulated more than 2-folds, whereas 10,010 genes were down-regulated more than 2-folds by $50\;{\mu}M$ allicin treatment. To confirm specific gene expressions, we performed RT-PCR. Consistent with the results of DNA microarray analysis, allicin dramatically induced ATF3 and NAG1 gene expression. Interestingly, NAG-1 protein expression was dependent on p53 presence. Taken together, our present results increase the knowledge of the molecular mechanism of anti-cancer and anti-proliferative activity mediated by allciin in human colorectal cancer cell.

• Journal of the Institute of Electronics Engineers of Korea CI
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• v.47 no.5
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• pp.17-24
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• 2010

Recently the study of identifying bio-markers for disease diagnosis and prognosis has been actively performed. In particular, lots of attentions have been paid to the finding of pathway gene-sets differentially expressed in disease patients rather than the finding of individual gene markers. In this paper we propose a novel method to identify disease-related pathway gene-sets based on time-series microarray data. For this purpose, we firstly compute individual gene scores by the using maSigPro (microarray Significant Profiles) and then arrange all the genes in the decreasing order of the corresponding gene scores. The rank of each gene in the entire list is used to evaluate the statistical significance of candidate gene-sets with Wilcoxson rank sum test. For the generation of candidate gene-sets, MSigDB (Molecular Signatures Database) pathway information has been employed. The experiment was conducted with prostate cancer time-series microarray data and the results showed the usefulness of the proposed method by correctly identifying 6 out of 7 biological pathways already known as being actually related to prostate cancer.

• Journal of Ginseng Research
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• v.41 no.1
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• pp.60-68
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• 2017

Background: Various Panax ginseng cultivars exhibit a range of diversity for morphological and physiological traits. However, there are few studies on diversity of metabolic profiles and genetic background to understand the complex metabolic pathway in ginseng. Methods: To understand the complex metabolic pathway and related genes in ginseng, we tried to conduct integrated analysis of primary metabolite profiles and related gene expression using five ginseng cultivars showing different morphology. We investigated primary metabolite profiles via gas chromatography-mass spectrometry (GC-MS) and analyzed transcriptomes by Illumina sequencing using adventitious roots grown under the same conditions to elucidate the differences in metabolism underlying such genetic diversity. Results: GC-MS analysis revealed that primary metabolite profiling allowed us to classify the five cultivars into three independent groups and the grouping was also explained by eight major primary metabolites as biomarkers. We selected three cultivars (Chunpoong, Cheongsun, and Sunhyang) to represent each group and analyzed their transcriptomes. We inspected 100 unigenes involved in seven primary metabolite biosynthesis pathways and found that 21 unigenes encoding 15 enzymes were differentially expressed among the three cultivars. Integrated analysis of transcriptomes and metabolomes revealed that the ginseng cultivars differ in primary metabolites as well as in the putative genes involved in the complex process of primary metabolic pathways. Conclusion: Our data derived from this integrated analysis provide insights into the underlying complexity of genes and metabolites that co-regulate flux through these pathways in ginseng.

• Tuberculosis and Respiratory Diseases
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• v.78 no.2
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• pp.99-105
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• 2015

Background: Aryl hydrocarbon receptor (AhR), a ligand-dependent transcription factor, binds to a wide variety of synthetic and naturally occurring compounds. AhR is involved in the regulation of inflammatory response during acute and chronic respiratory diseases. We investigated whether nuclear receptor coactivator 7 (NCOA7) could regulate transcriptional levels of AhR target genes and inflammatory cytokines in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-treated human bronchial epithelial cells. This study was based on our previous study that NCOA7 was differentially expressed between normal and chronic obstructive pulmonary disease lung tissues. Methods: BEAS-2B and A549 cells grown under serum-free conditions were treated with or without TCDD (0.15 nM and 6.5 nM) for 24 hours after transfection of pCMV-NCOA7 isoform 4. Expression levels of cytochrome P4501A1 (CYP1A1), IL-6, and IL-8 were measured by quantitative real-time polymerase chain reaction. Results: The transcriptional activities of CYP1A1 and inflammatory cytokines were strongly induced by TCDD treatment in both BEAS-2B and A549 cell lines. The NCOA7 isoform 4 oppositely regulated the transcriptional activities of CYP1A1 and inflammatory cytokines between BEAS-2B and A549 cell lines. Conclusion: Our results suggest that NCOA7 could act as a regulator in the TCDD-AhR signaling pathway with dual roles in normal and abnormal physiological conditions.

• Journal of Veterinary Clinics
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• v.19 no.3
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• pp.299-302
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• 2002

Selectins are differentially expressed carbohydrate binding proteins involved in the initiation of tissue inflammation by mediating the rolling and tethering of leukocytes on the vascular endothelium. This primary event in initiation of inflammation, as occurs during reperfusion injury, can be therapeutically targeted using selectin inhibitors, which generally block binding of sLex to E-, P-, and L-selectins. The objective of this study was to determine the role of selectins in renal ischemia/reperfusion injury after kidney transplantation. Canine kidneys were subjected to 60-min warm ischemia, flushed with UW solution, cold stored for 24 h, and autotransplanted into the nephrectomized donor. Renal autografts were monitored for 7 days by serum creatinine in the first study and by histology and myeloperoxidase activity after 4-hour reperfusion in the second study. In each study, one group of animals received TBC1269 (selectin inhibitor) and the other received saline vehicle. Serum creatinine rose quickly after transplantation and was not different between the groups. TBC1269 abolished a reperfusion-induced 2-fold increase in renal cortex neutrophil infiltration and improved histologic signs of ischemia after 4 hours of reperfusion. Selectin blockade does not improve the course of injury caused by warm renal ischemia. A minor benefit associated with the inhibition of early inflammation during reperfusion after kidney transplantation seems to occur.