• Title/Summary/Keyword: Gap Junctional Intercellular Communication (GJIC)

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Involvement of P38 Mapk and Gap Junctional Intercellular Communication (Gjic) in 12-O-Tetradecanoyl Phorbol 13-Acetate-Induced Stellation of Neurosphere-Derived Cells

  • Yang, Se-Ran;Ahn, Nam-Shik;Jung, Ji-Won;Park, Joon-Suk;Yoon, Byoung-Su;Lee, Yong-Soon;Kang, Kyung-Sun
    • Proceedings of the Korean Society of Toxicology Conference
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    • pp.123-123
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    • 2003
  • Primary cultures of rat fetus brain exhibit phenotypes of neuron, oligodendrocyte, and astrocyte from "neurospheres". To understand the role of mitogen-activated protein kinase (MAPK) cascade and gap junctional intercellular communication (GJIC) in the differentiation of neurosphere-derived astrocyte, we investigated the effects of 12-O-tetradecanoylphorbol-13-acetate (TPA) on the cultured astrocyte morphology.(omitted)

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Effects of Airborne Samples Collected in Yeochun on Gap Junctional Inter cellular Communication in WBF-344 Rat Liver Epithelial Cells (여천공단 일부지역의 대기오염물질이 WBF-344간 상피세포의 Gap Junctional Intercellular Communication에 미치는 영향)

  • 양재만;박재학;김윤신;이영순
    • Journal of Korean Society for Atmospheric Environment
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    • v.13 no.3
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    • pp.207-214
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    • 1997
  • We collected airborne complex mixtures in a industrial area of Yeochun, and examined whether these complex mixtures could affect gap junctional intercellular communication (GJIC) in a cultured WBF-344 rat liver epithelial cells (LEC). Since the reduction of GJIC plays an important role in chemical carcinogenesis, measurement of changes of GJIC is a meaningful method to screen carcinogenicity of these mixtures. High and low volume samples were dissolved in dimethyl sulfoxide (DMSO) and tested. Blank filter extractions were also examined for exclud-ing possible toxicity of filter itself, and TPA (12-O-tetradecanoylphorbol-13-acetate) and DMSO were used as positive and negative control, respectively. When the cells were exposed to samples at concentration below that required to maintain rather than 85% cell viability based on the result of neutral red uptake assay, maximal inhibition of GJIC was observed at 1hr after treatment with both high and low volume samples by scrape-loading dye transfer assay. In fluorescence recovery after photobleaching assay, recovery rates via gap junctions were 33%/min in high volume sample and 62%/min in low volume sample. In together, airborne samples collected in Yeochun inhibited GJIC in a cultured WBF-344 rat LEC. These results suggest airborne samples tested in this experiment may attribute to cause a certain type and degree of cancers in in vivo when exposured for some periods.

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Investigation of Carcinogenic Potential of TCDD in the Human Breast Epithelial Cell line (사람의 유방상피세포에서 TCDD에 의한 발암성 연구)

  • 김정환;나혜경;서영준
    • Environmental Mutagens and Carcinogens
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    • v.22 no.4
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    • pp.312-318
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    • 2002
  • Dioxin represents a group of halogenated aromatic hydrocarbons of which 2,3,7,8-tetrachlorod-ibenzo-p-dioxin (TCDD) is well known for its extremely toxic properties as well as ubiquitous presence in our environment and ecosystems. In order to better assess the carcinogenic mechanism of dioxin, we should utilize the reliable biomarkers that can precisely and correctly reflect multi-stage carcinogenesis. When MCF10A cells were exposed to TCDD (10 nM), expression of both CYP1A1 and CYP1B1 was induced in a time-related manner. The expression as well as activity of ornithine decarboxylase was transiently induced by TCDD treatment. In contrast, the induction of COX-2 that is implicated in carcinogenesis as well as inflammation, was not induced by TCDD. In another study, gap-junctional intercellular communication (GJIC) was attenuated by TCDD treatment as revealed by the dye-transfer assay. Based on these findings, TCDD has both tumor initiating and promoting potential in human breast epithelial cells in culture. Also, treatment of MCF10A cells with the carcinogen 7,12-dimethylbenz[a]anthracene plus TCDD resulted in malignant cell transformation as revealed by increased anchorage-independent growth of exposed cells. Additional studies may be necessary to assess the effects of TCDD on multi-stage carcinogenesis in vivo.

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Toxicity and Carcinogenicity of Dichlorodiphenyltrichloroethane (DDT)

  • Harada, Takanori;Takeda, Makio;Kojima, Sayuri;Tomiyama, Naruto
    • Toxicological Research
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    • v.32 no.1
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    • pp.21-33
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    • 2016
  • Dichlorodiphenyltrichloroethane (DDT) is still used in certain areas of tropics and subtropics to control malaria and other insect-transmitted diseases. DDT and its metabolites have been extensively studied for their toxicity and carcinogenicity in animals and humans and shown to have an endocrine disrupting potential affecting reproductive system although the effects may vary among animal species in correlation with exposure levels. Epidemiologic studies revealed either positive or negative associations between exposure to DDT and tumor development, but there has been no clear evidence that DDT causes cancer in humans. In experimental animals, tumor induction by DDT has been shown in the liver, lung, and adrenals. The mechanisms of hepatic tumor development by DDT have been studied in rats and mice. DDT is known as a non-genotoxic hepatocarcinogen and has been shown to induce microsomal enzymes through activation of constitutive androstane receptor (CAR) and to inhibit gap junctional intercellular communication (GJIC) in the rodent liver. The results from our previously conducted 4-week and 2-year feeding studies of p,p'-DDT in F344 rats indicate that DDT may induce hepatocellular eosinophilic foci as a result of oxidative DNA damage and leads them to hepatic neoplasia in combination with its mitogenic activity and inhibitory effect on GJIC. Oxidative stress could be a key factor in hepatocarcinogenesis by DDT.

Ginseng Saponin as an Antagonist for Gap Junctional Channels

  • Rhee, Seung-Keun
    • Journal of Ginseng Research
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    • v.30 no.2
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    • pp.64-69
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    • 2006
  • Gap junctional channels, allowing rapid intercellular communication and synchronization of coupled cell activities, play crucial roles in many signaling processes, including a variety of cell activities. Consequently, a modulation of the gap junctional intercellular communication (GJIC) should be a potential pharmacological target. In the present, the GJIC of a epithelial-derived rat mammary cells (BICR-M1Rk) was assessed in the presence of ginseng saponin, by using an established method of scrape-loading dye transfer assay. The transfer of Lucifer yellow (diameter: 1.2 nm) among the neighboring BICR-M1Rk cells, in which connexin43 (Cx43) is a major gap junction channel-forming protein, was significantly retarded at a concentration of $10{\mu}g/ml$ ginseng saponin. By using both methods of RT-PCR and Western blotting, it was demonstrated that ginseng saponin modulated neither the mRNA synthesis of Cx43 nor the translational process of Cx43. This ginseng saponin-induced modification of GJIC was a similar phenomenon observed under the $\beta$-glycyrrhetinic acid treatment, a well-known gap junction channel blocker. Taken together, it is reasonable to conclude that the ginseng saponin inhibits GJIC only by modulating the gating property of gap junction channels.

Inhibition of Gap Junctional Intercellular Communication in Rat Liver Epithelial Cells Induced by BHT and Propyl Gallate (간상피세포에서 BHT와 propyl gallate에 의한 gap junctional intercellular communication 억제 효과)

  • Kim, Ji-Sun;Kim, Sung-Ran;Ahn, Ji-Yun;Ha, Tae-Youl;Kang, Kyoung-Sun;Kim, Sun-A
    • Korean Journal of Food Science and Technology
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    • v.39 no.5
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    • pp.558-563
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    • 2007
  • This study was conducted to analyze the cytotoxic effects of butylated hydroxytoluene (BHT) and propyl gallate (PG) in WB-F344 rat liver epithelial cells. Here we measured the inhibition level of gap junctional intercellular communication (GJIC) and elucidated the relationships between GJIC and mitogen-activated protein kinases (MAPKs) such as ERK, JNK, and p38. The cytotoxicities of BHT and PG appeared at concentrations of 1.0mM and 0.25mM, respectively, in the WB-F344 cells; and GJIC inhibition, which was analyzed by a scrape-loading/dye transfer assay and Western blotting analysis, appeared at 0.6mM for BHT and 0.1mM for PG, respectively. Also, the phosphorylations of Cx43, ERK, JNK, and p38 increased in dose-dependent manners. This suggests that BHT and PG treatments inhibited GJIC by the phosphorylation of MAPKs prior to cell damage.

PREVENTIVE EFFECT OF MUSHROOM PHELLINUS LINTEUS ON THE INHIBITION OF GAP JUNCTIONAL INTERCELLULAR COMMUNICATION BY $H_2O_2$ IS INVOLVED IN THE UP-REGULATION OF ERK2 AND p38

  • Kang, Kyung-Sun;Cho, Jong-Ho;Cho, Sung-Dae;Kim, Kyung-Bae;Lee, Ji-Hae;Ahn, Nam-Shik;Jung, Ji-Won;Yang, Se-Ran;Park, Joon-Suk;Yoon, Byung-Su;Kim, Sung-Hoon;Lee, Yong-Soon
    • Proceedings of the Korean Society of Toxicology Conference
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    • pp.159-160
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    • 2001
  • Gap junctional intercellular communication (GJIC) is a cellular event underlying the tumor promotion process and that treatment to prevent the down-regulation or to up-regulate GJIC is important in preventing tumor promotion. We evaluated the potential preventive effect of Mushroom Phellinus Linteus (PL) against the promoting action of hydrogen peroxide ($H_2O$$_2$) in WB-F344 rat liver epithelial cells.(omitted)

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Protective Effects of Lipophilic Extracts from Different Colored Paprikas on Inhibition of $H_2O_2$-induced Gap Junctional Intercellular Communications ($H_2O_2$로 유도된 WB-F344 세포의 GJIC 억제에 대한 색상별 파프리카 추출물의 보호 효과)

  • Kim, Ji-Sun;Kim, Suna
    • Journal of the East Asian Society of Dietary Life
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    • v.24 no.3
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    • pp.359-367
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    • 2014
  • This study analyzed phytochemicals, including various carotenoids, tocopherol and L-ascorbic acid, in green, yellow and orange paprikas (GP, YP and OP) and measured the preventive effects of lipophilic extracts from different colored paprikas on the blockage of gap junctional intercellular communication (GJIC), which is known as a cellular event associated with tumor promotion. Main carotenoids were lutein and ${\beta}$-carotene in GP, lutein, ${\beta}$-carotene, capsanthin, violaxanthin, ${\beta}$-carotene and capsorubin in YP, and lutein, ${\beta}$-carotene, cryptoxanthin and zeaxanthin in OP. Total carotenoid contents were $65.54{\pm}15.87$ mg/100 g dw in OP, $11.98{\pm}0.69$ mg/100 g dw in YP and $10.30{\pm}1.43$ mg/100 g dw in GP. Tocopherol contents were highest in GP compared with in YP and OP, whereas L-ascorbic acid contents were very high in all paprikas. We determined the non-cytotoxic levels of paprika extracts by MTT assay, which showed less formation of reactive oxygen species (ROS) induced by $500{\mu}M$ $H_2O_2$ for 1h. Finally, we showed that pretreatment of paprika extracts prevented inhibition of GJIC induced by $500{\mu}M$ $H_2O_2$ by the scrape-loading/dye-transfer technique. In conclusion, each colored paprika has unique phytochemicals and showed a protective effect on inhibition of GJIC.

Determination of Flavonoids from Allium victorialis var. platyphyllum and Their Effect on Gap Junctional Intercellular Communication

  • Hong, Eun-Young;Choi, Soo-Im;Kim, Gun-Hee
    • Food Science and Biotechnology
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    • v.16 no.5
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    • pp.747-752
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    • 2007
  • This study was carried out to identify and quantify the flavonoids from 6 different plant parts of Allium victorialis var. platyphyllum (AVP), including the flower, leaf, root, stem, flower stalk, and flower seed, using liquid chromatography/ mass spectrometry. Two major flavonoids were structurally identified as quercetin (3,5,7,3'4,'-pentahydroxyflavone) and kaempferol (3,5,7,4'-tetrahydroxyflavone) at contents of 11.8-25.8 and $6.0-64.4\;{\mu}g/mL$, respectively. In particular, the flower and root plant parts contained the highest amounts of quercetin and kaempferol compared to the other parts. We also assessed the recovery effects of each plant-part extract of AVP on gap junctional intercellular communication (GJIC) in WB-F344 cells by the scrape-loading and dye transfer (SL/DT) method. According to the results, GJIC was reduced by approximately 70.2% ($62.3{\pm}12.5$ cells) compared to the control ($209{\pm}9.5$ cells, 100%) when 12-O-tetradecanoylphorbol-13-acetate (TPA) was treated alone in the WB-F344 rat liver epithelial cells. However, the stem extract (0.2 mg/mL) restored GJIC to basal levels (92%, $204{\pm}2.3$ cells, p<0.01) and the flower extract (0.2 mg/mL) stimulated GJIC to 82.5% ($172.6{\pm}8.3$ cells, p<0.05), when applied together with the TPA.