• Genomics & Informatics
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• v.10 no.1
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• pp.16-22
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• 2012

Autosomal dominant polycystic kidney disease (ADPKD) is characterized by formation of multiple fluid-filled cysts that expand over time and destroy renal architecture. The proteins encoded by the $PKD1$ and $PKD2$ genes, mutations in which account for nearly all cases of ADPKD, may help guard against cystogenesis. Previously developed mouse models of $PKD1$ and $PKD2$ demonstrated an embryonic lethal phenotype and massive cyst formation in the kidney, indicating that $PKD1$ and $PKD2$ probably play important roles during normal renal tubular development. However, their precise role in development and the cellular mechanisms of cyst formation induced by $PKD1$ and $PKD2$ mutations are not fully understood. To address this question, we presently created $Pkd2$ knockout and $PKD2$ transgenic mouse embryo fibroblasts. We used a mouse oligonucleotide microarray to identify messenger RNAs whose expression was altered by the overexpression of the $PKD2$ or knockout of the $Pkd2$. The majority of identified mutations was involved in critical biological processes, such as metabolism, transcription, cell adhesion, cell cycle, and signal transduction. Herein, we confirmed differential expressions of several genes including aquaporin-1, according to different $PKD2$ expression levels in ADPKD mouse models, through microarray analysis. These data may be helpful in $PKD2$-related mechanisms of ADPKD pathogenesis.

• International Journal of Oral Biology
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• v.37 no.2
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• pp.51-56
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• 2012

Tooth development involves bud, cap, bell and hard tissue formation stages, each of which is tightly controlled by regulatory molecules. The aim of this study was to identify genes that are differentially expressed during dental hard tissue differentiation. Sprague-Dawley rats at postnatal days 3, 6 and 9 were used in the analysis. Differential display RT-PCR (DD-PCR) was used to screen differentially expressed genes between the 2nd (root formation stage, during mineralization) and 3rd (cap stage, before mineralization) molar germs at postnatal day 9. The DNA detected in the 2nd molar germs showed homology to osteonectin only (GenBank accession no. NM_012656.1). The level of osteonectin mRNA expression was much higher in the 2nd molar germs than in the 3rd molar germs and was found to increase in a time-dependent manner from the early bell stage to the root formation stage in the 2nd molar germs. The pattern of osteonectin protein expression was consistent with these RT-PCR results. Osteonectin protein was found by immunofluorescent analysis to localize in odontoblasts and preodontoblasts rather than the dentin matrix itself. Further studies are needed to validate the involvement of osteonectin in mineralization and root formation.

• Journal of Plant Biotechnology
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• v.30 no.2
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• pp.201-206
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• 2003

Differential responses of red pepper plant and cultured cells to enhanced ${\gamma}$-ray($^{60}$ Co) and ultraviolet(UV) stress were investigated. In seed treatment, 1 Gy of ${\gamma}$-ray increased seedling dry weight up to 19.1%, but 50 Gy treatment markedly ingibited seed germination and subsequent growth of seedling. UV treatment to seed did not change the germination ability of seeds and the growth of seedlings regardless of duration of UV treatment until 24 hrs. In case of UV treatment to seedlings, plant injury was seriously progressed even after the seedlings were returned to no UV condition, and eventually all the leaves showed chlorosis by the stress. However, progress of plant injury by ${\gamma}$-ray stress slower than that caused by UV stress, and even at the high dose of ${\gamma}$-ray 50 Gy, did not caused the cholrosis of stressed plant leaf. Amount of electrolytes leakage from plant leaf by UV treatment for 24hrs was increased up to 28.8 folds in comparison with untreated control, whereas that of 50 Gy of ${\gamma}$-ray was increased only 1.2 folds. UV stress induced the production of capsidiol, antimicrobial phytoalexin, by activation of gene expression involved in capsidiol biosynthesis, such as sesquiterpene cyclase and cyclase and cytochrome P450 hydroxylase in the leaf and cultured cell, but ${\gamma}$-ray stress induced neither the production of capsidiol nor expression of the genes.

• Molecular & Cellular Toxicology
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• v.5 no.4
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• pp.310-316
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• 2009

Some environmental chemicals have been shown to cause liver-toxicity as the result of bioaccumulation. Particularly, fungicides have been shown to cause varying degrees of hepatictoxicity and to disrupt steroid hormone homeostasis in in vivo models. The principal objective of this study was to evaluate the liver-toxic responses of environmental chemicals-in this case selected fungicides and parasiticides-in order to determine whether or not this agent differentially affected its toxicogenomic activities in hepatic tumor cell lines. To determine the gene expression profiles of 3 fungicides (triadimefon, myclobutanil, vinclozolin) and 1 parasiticide (dibutyl phthalate), we utilized a modified HazChem human array V2. Additionally, in order to observe the differential alterations in its time-dependent activities, we conducted two time (3 hr, 48 hr) exposures to the respective IC20 values of four chemicals. As a result, we analyzed the expression profiles of a total of 1638 genes, and we identified 70 positive significant genes and 144 negative significant genes using four fungicidic and parasiticidic chemicals, using SAM (Significant Analysis of Microarray) methods (q-value<0.5%). These genes were analyzed and identified as being related to apoptosis, stress responses, germ cell development, cofactor metabolism, and lipid metabolism in GO functions and pathways. Additionally, we found 120 genes among those time-dependently differentially expressed genes, using 1-way ANOVA (P-value<0.05). These genes were related to protein metabolism, stress responses, and positive regulation of apoptosis. These data support the conclusion that the four tested chemicals have common toxicogenomic effects and evidence respectively differential expression profiles according to exposure time.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.5
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• pp.2175-2178
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• 2012

Purpose: Definite diagnosis of follicular thyroid carcinoma (FTC) is based on the presence of capsular or vascular invasion. To date, no reliable and practical method has been introduced to discriminate this malignant neoplasm from follicular thyroid adenoma (FTA) in fine needle aspiration biopsy material. Matrix metalloproteinase-2 (MMP-2), by degrading extracellular matrix, and caspase-3, by induction of apoptosis, have been shown to play important roles in carcinogenesis and aggressive behavior in many tumor types. The aim of this study was to examine expression of MMP-2 and caspase-3 in thyroid follicular neoplasms and to determine their usefulness for differential diagnosis. Method: Sixty FTAs and 41 FTCs were analysed immunohistochemically for MMP-2 and caspase-3. Result: MMP-2 was positive in 4 FTCs (9.8%), but in none of FTAs, with statistical significance (p= 0.025). Caspase-3 was positive in 30 (50%) of FTAs and in 27 (65.9%) of FTCs. Conclusion: Our results show MMP-2 expression only in FTCs and suggest that this protein may be a useful marker to confirm diagnosis of FTC versus FTA with 100% specificity and 100% predictive value of a positive test. We failed to show any differential diagnostic value for caspase-3 in thyroid follicular neoplasms.

• Proceedings of the Korea Society of Environmental Toocicology Conference
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• 2003.10a
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• pp.172-172
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• 2003

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a prototype of many halogenated aromatic hydrocarbons, is a ubiquitous, persistent environmental contaminant and displays high toxicity in animals and has been implicated in human carcinogenesis. Although the mechanism of carcinogenesis by TCDD is unclear, it is considered to be a non-genotoxic and tumor promoter. In this study, we investigated the tumor promotion effect of TCDD on the two-stage skin chemical carcinogenesis using hairless mouse (SKH1). We induced papillomas after treatment with N-methyl -N'-nitro-N-nitorsoguanidine (MNNG) as a initiator and TCDD as a promoter for 30 weeks. We found that the incidence or multiplicity of papillomas and hyperplastic nodules was maximally induced at MNNG-TCDD group compare to control, MNNG, and TCDD alone. These results suggesting that TCDD can acts as a potent promoter in the hairless mouse skin. In addition, we used cDNA microarray to detect the differential gene expression in normal, tumor surrounding, and tumor regions induced in hairless mouse skin by MNNG plus TCDD protocol. We found that 49 and 42 genes out of 5,592 genes associated with protein synthesis, cell organization, lipid transport and oxidative stress in tumor and surrounding regions were up- or down- regulated two fold or more, respectively. We are currently investigating how these genes play a role in TCDD-mediated chemical carcinogenesis.

• Korean Journal of Plant Tissue Culture
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• v.28 no.5
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• pp.231-237
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• 2001

A cDNA clone encoding metallothionein-like protein (CitMT45), which was reported by Moriguchi et al. (1998), was isolated from Citrus fruits cDNA library through differential screening. Our cDNA clone has longer 5'untranslated region, compared to it isolated by Moriguchi et al. (1998). RNA blot analysis showed that the mRNA was abundant in fleshes than peels, leaves, and flowers, as a single transcript. However, regardless of tissue types, the blots showed the similar expression patterns in the process of development with some different profile. These results suggest that CitMT45 may play important roles in the development and/or senescence of various tissues of Citrus. A genomic clone corresponding to CitMT45 was isolated and found to have three exons and two introns. A primer extension analysis suggested that the transcription of CitMT45 gene was started at three start sites with different degrees. The 5'-flanking region was shown to contain a putative metal regulatory element (MRE) and low- temperature responsive element which suggests the possibility of metal-and cold-regulated transcription, respectively.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2007.04a
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• pp.147-153
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• 2007

Central to developing new treatment strategies for late onset sporadic Parkinson's disease (PD) and early onset familial PD is resolving the enigma of the specific vulnerability exhibited by substantia nigra dopamine (DA) neurons despite multiple risk factors. Neuropathological evidence from both human and experimental models of PD firmly supports a significant role for oxidative stress (OS) and mitochondrial dysfunction in the death of nigral DA neurons. Largely unknown are the genes underlying selective susceptibility of nigral DA neuron to OS and mitochondrial dysfunction and how they effect nigral DA cell death. To overcome the paucity of nigral DA neurons as well as the dilution effect of non-DA cells in brain tissues, we have developed wild type DA cell line model, SN4741 and mutant DJ-1 (-/-) DA cells, appropriate for microarray analysis and differential mitochondrial proteomics. Mutations in the DJ-1 gene (PARK7), localized in cytoplasm and mitochondria, cause autosomal recessive early onset PD. Through microarray analysis using SN4741 cells followed by validation tests, we have identified a novel phylogenically conserved neuroprotective gene, Oxi-a, which is specifically expressed in DA neurons. The knockdown of the gene dramatically increased vulnerability to as. Importantly as down-regulated the expression level of the gene and recovery of its expression via transient transfection exerted significant neuroprotection against as insult. We also have identified altered expression of mitochondrial proteins and other familial PD genes in DJ-1 (-/-) mutant cells by differential mitochondrial proteomics. In DJ-1 (-/-) cells the knockdown of the other familial PD genes (Parkin and PINK1) dramatically increased susceptibility to as. Thus, further functional characterization of the Oxi-$\alpha$ gene family and the mitochondrial alteration in the DJ-1 (-/-) cell model will provide the rationale for the neuroprotective therapy against both sporadic and familial PD.

• Journal of Plant Biology
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• v.38 no.4
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• pp.381-388
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• 1995

Four cONA clones expressed in late root nodules of Canavalia lineata were isolated by differential screening using total RNA from uninfected roots, Clb1 and uricase II cONAs as competitors and named Cnod1, Cne2, Cne3 and Clb2, respectively. Cnod1, hybridized to 1450 nt mRNA, was highly homologous to cysteine proteinase gene from rice and showed nodule-specific expression, especially in late nodules. Cne2, hybrdized to 900 nt mRNA, was moderately homologous to Expressed Sequence Tag of rice and expressed mainly in root nodules. Its expression was increased at 13 OAI and subsequently remained at the same level. Cne3, hybridized to 1700 nt and 1400 ot mRNAs, was highly homologous to tonoplast membrane intrinsic protein TRG31 gene from pea and was expressed strongly in roots and nodules, but weakly in leaves. Temporal expression pattern of Cne3 was coincided with the life cycle of root nodules. Clb2, hybridized to 800 nt mRNA, was expressed from 8 OAI, amplified at 13 DAI and remained steady thereafter.eafter.

• Journal of Veterinary Science
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• v.22 no.5
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• pp.61.1-61.13
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• 2021

Background: Hepatocellular carcinoma is the most common primary hepatic malignancy in humans and dogs. Several differentially expressed molecules have been studied and reported in human hepatocellular carcinoma and non-neoplastic liver lesions. However, studies on the features of canine hepatocellular carcinoma are limited, especially related to the differential characteristics of neoplastic and non-neoplastic lesions. Objectives: The study's objective was 1) to examine and evaluate the expression of arginase-1, P-glycoprotein, and cytokeratin 19 in canine liver tissues and 2) to investigate the differential features of hepatocellular carcinomas, liver tissue with non-neoplastic lesions, and paracancerous liver tissues in dogs. Methods: The expression levels of three markers underwent immunohistochemical analysis in 40 non-neoplastic liver tissues, 32 hepatocellular carcinoma tissues, and 11 paracancerous liver tissues. Scoring of each marker was performed semi-quantitatively. Results: Arginase-1 and P-glycoprotein were significantly downregulated in hepatocellular carcinoma, compared with hepatic tissues with non-neoplastic diseases (p < 0.001). Expression levels of arginase-1 and P-glycoprotein were also significantly lower in hepatocellular carcinoma than in paracancerous liver tissues (arginase-1, p = 0.0195; P-glycoprotein, p = 0.047). Few cytokeratin 19-positive hepatocytes were detected and only in one hepatocellular carcinoma and one cirrhotic liver sample. Conclusions: The results of this study suggest that downregulation of arginase-1 and P-glycoprotein is a feature of canine hepatocellular carcinoma; thus, those markers are potential candidates for use in differentiating hepatocellular carcinomas from non-neoplastic liver lesions in dogs.