Eui-Bae Jeung

Chungbuk National University, Chinsen, Chungcheongbuk-do, South Korea

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Publications (192)506.39 Total impact

  • Dongoh Lee · Changhwan Ahn · Beum-Soo An · Eui-Bae Jeung ·

    International Journal of Environmental Research and Public Health 11/2015; 12(11):14610-14625. DOI:10.3390/ijerph121114610 · 2.06 Impact Factor
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    ABSTRACT: The establishment of porcine embryonic stem cells (ESCs) would have great impact in biomedical studies and preclinical trials through their use in genetic engineering. However, authentic porcine ESCs have not been established until now. In this study, a total of seven putative ESC lines were derived from porcine embryos of various origins, including in vitro fertilization, parthenogenetic activation, and, in particular, induced pluripotent stem (iPS) nuclear transfer (NT) from a donor cell with induced pluripotent stem cells (iPSCs). To characterize these cell lines, several assays including an assessment of intensive alkaline phosphatase activity, karyotyping, embryoid body formation, expression analysis of the pluripotency-associated markers, and the three germ layerassociated markers were performed. Based on quantitative polymerase chain reaction, the expression levels of REX1 and FGFR2 in iPS-NT lines were higher than those of cells of other origins. Additionally, only iPS-NT lines showed multiple aberrant patterns of nuclear foci elucidated by immunofluorescence staining of H3K27me3 as a marker of the state of X chromosome inactivation and a less mature form of mitochondria like naive ESCs, by transmission electron microscopy. Together, these data suggested that established putative porcine ESC lines generally exhibited a primed pluripotent state, like human ESCs. However, iPS-NT lines have especially unique characteristics distinct from other origins because they have more epigenetic instability and naive-like mitochondrial morphology than other putative ESC lines. This is the first study to establish and characterize the iPSC-derived putative ESC lines and compare them with other lines derived from different origins in pigs.
    Theriogenology 11/2015; DOI:10.1016/j.theriogenology.2015.09.051 · 1.80 Impact Factor
  • Yeon Woo Jeong · Joung Joo Kim · Hyun Duk Kim · Kyu Chan Hwang · Sang Hwan Hyun · Nam-Hyung Kim · Eui-Bae Jeung · Woo Suk Hwang ·

    Theriogenology 10/2015; DOI:10.1016/j.theriogenology.2015.10.026 · 1.80 Impact Factor
  • Changhwan Ahn · Da-Hye Shin · Dongoh Lee · Hee Young Kang · Eui-Bae Jeung ·

    09/2015; 16(3):98-103. DOI:10.12729/jbr.2015.16.3.098
  • Source
    Yeong-Min Yoo · Eui-Man Jung · Kyung-Chul Choi · Eui-Bae Jeung ·

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    ABSTRACT: Fucoidan which is sulfated polysaccharide extracted from brown seaweed has a wide variety of internal biological activities. The objectives of this study were to examine the effect of fucoidan on nitric oxide (NO) production in lipopolysaccharide (LPS)-stimulated porcine peripheral blood mononuclear cells (PBMCs) and to investigate whether this effect is involved in the expression of inducible nitric oxide synthase (iNOS) and the activation of activator portein-1 (AP-1). The levels of NO production and AP-1 activity in the culture supernatants from porcine PBMCs were measured by the enzyme-linked immunosorbent assay and the levels of iNOS and AP-1 mRNA were determined by real time polymerase chain reaction. Fucoidan in LPS-naïve PBMCs has no effects on the production of NO and activity of AP-1. Expressions of iNOS and AP-1 mRNA in LPS-naïve PBMCs were also not affected by treatment of fucoidan. However, NO production, AP-1 activity and expressions of iNOS and AP-1 mRNA were dramatically increased in PBMCs stimulated with LPS. Enhancing effects of NO production and AP-1 activity in PBMCs induced by LPS were reduced by addition of fucoidan. Fucoidan also inhibited an increase in expressions of iNOS and AP-1 mRNA in LPS-stimulated PBMCs. These results suggested that fucoidan exerts anti-inflammatory effect by down-regulating production of NO via suppressing expression of iNOS and activity of AP-1 in LPS-stimulated porcine PBMCs. © 2015 Korean Society of Veterinary Clinics. All rights reserved.
    Journal of Veterinary Clinics 08/2015; 32(4):289. DOI:10.17555/jvc.2015.
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    ABSTRACT: 2-Methoxyestradiol (2-ME), an endogenous metabolite of 17β-estradiol (E2), interacts with estrogen receptors (ERs) and microtubules, however, 2-ME has a low affinity for ERs. Furthermore, 2‑ME has been identified as a potential novel antitumor agent, combining its anti‑proliferative effects on a variety of tumor cell types with its anti‑angiogenic action. Therefore, 2‑ME is of interest due to its potential anticancer therapeutic effects. In the current study, the estrogenic effect of 2‑ME on CaBP‑9k, ERα, and progesterone receptor (PR) mRNA levels in the absence and presence of E2 and progesterone (P4) in in vivo and in vitro models was examined. In GH3 cells, the mRNA level of CaBP‑9k was induced in the E2 treatment group (concentration, 10‑9 M), and the expression of CaBP‑9k was also upregulated in the 2‑ME‑treated group (concentration, 10‑7 M). Uterine lactoferrin (Ltf) mRNA expression was also increased in the 2‑ME group [dose, 40 mg/kg body weight (BW)], which was comparable to the response with E2 (dose, 40 µg/kg BW) observed in mice. As inhibitors of ER and PR activity, ICI 182,780 and mifepristone (RU486) were observed to reverse the E2 or 2‑ME mediated increase of CaBP‑9k and Ltf mRNA expression. In addition, it was found that 2‑ME significantly decreased the levels of ERα and increased PR transcripts. Consistent with the in vitro results, the mRNA levels revealed decreased ERα and increased PR in in vivo treatment of E2 and 2‑ME. These findings demonstrate that the expression of estrogenic markers, CaBP‑9k and Ltf, is regulated by 2‑ME in in vitro and in vivo models, therefore, estrogenic activi-ties of 2-ME may be increased in females during the estrous cycle via the ER and/or PR-mediated signaling pathway.
    Molecular Medicine Reports 07/2015; 12(4). DOI:10.3892/mmr.2015.4073 · 1.55 Impact Factor
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    ABSTRACT: Alkylphenols such as 4-tert-octylphenol (OP), nonylphenol, and bisphenol A are classified as endocrine-disrupting chemicals (EDCs). Digestion and metabolism of food are controlled by many endocrine factors, including insulin, glucagon, and estrogen. These factors are differentially regulated during pregnancy. The alteration of nutritional intake and fat metabolism may affect the maintenance of pregnancy and supplementation of nutrients to the fetus, and therefore can cause severe metabolic diseases such as ketosis, marasmus and diabetes mellitus in pregnant individuals. In this study, we examined the effects of OP on fat metabolism in pregnant rats. Ethinyl estradiol (EE) was also administered as an estrogenic positive control. In our results, rats treated with OP showed significantly reduced body weights compared to the control group. In addition, histological analysis showed that the amount of fat deposited in adipocytes was reduced by OP treatment. To study the mechanism of action of OP in fat metabolism, we examined the expression levels of fat metabolism-associated genes in rat adipose tissue and liver by real-time PCR. OP and EE negatively regulated the expression of lipogenic enzymes, including FAS (fatty acid synthase), ACC-1 (acetyl-CoA carboxylase-1), and SCD-1 (stearoyl-CoA desaturase-1). The levels of lipogenic enzyme-associated transcription factors such as C/EBP-α (CAAT enhancer binding protein alpha) and SREBP-1c (sterol regulatory element binding protein-1c) were also reduced in both liver and adipose tissue. In summary, these findings suggest that OP has adverse effects on fat metabolism in pregnant rats and inhibits fat deposition via regulating lipogenic genes in the liver and adipose tissue. The altered fat metabolism by OP may affect the nutrition balance during pregnancy and can cause metabolism-related diseases. Copyright © 2015 Elsevier B.V. All rights reserved.
    06/2015; 40(1):284-291. DOI:10.1016/j.etap.2015.06.020
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    ABSTRACT: Granulocyte colony-stimulating factor (G-CSF) is required for proliferation, differentiation, and survival of cells. It is also a biomarker of human oocyte developmental competence for embryo implantation. In humans, the G-CSF concentration peaks during the ovulatory phase of the ovarian cycle. In this study, the expressions of G-CSF and its receptor were analyzed by polymerase chain reaction in granulosa cells (GCs), CL, cumulus cells (CCs), and oocytes. Cumulus-oocyte complexes were aspirated from antral follicles of 1 to 3 mm (small follicles) and 4 to 6 mm (medium follicles). Cumulus-oocyte complexes from two kinds of follicles were matured in protein-free maturation medium supplemented with various concentrations of G-CSF (0, 10, and 100 ng/mL). By real-time polymerase chain reaction, the expressions of G-CSF and its receptor were detected in GCs, CL, CCs, and oocytes. Interestingly, the G-CSF transcript levels were significantly lower in oocytes than in the other cell types, whereas the G-CSF receptor transcript levels in oocytes were similar to those in GCs. After 44 hours of IVM, no differences in the rate of nuclear maturation were detected; however, the intracellular reactive oxygen species levels in oocytes from both groups of follicles matured with 10 ng/mL of human recombinant G-CSF (hrG-CSF) groups were significantly lower (P < 0.05). After parthenogenetic activation, the cleavage rates were significantly (P < 0.05) higher in 100 ng/mL hrG-CSF-treated small (63.3%) follicles than in 0, 10 ng/mL hrG-CSF-treated small (38.6% and 49.0%, respectively) follicles and 0 ng/mL hrG-CSF-treated medium (52.1%) follicles, and the cleavage rates were significantly (P < 0.05) higher in 10 ng/mL hrG-CSF-treated medium (76.3%) follicles than in all other groups. The blastocyst formation rates were significantly (P < 0.05) higher in 100 ng/mL hrG-CSF-treated small (31.2%) follicles than in 0 and 10 ng/mL hrG-CSF small (10.4% and 15.6%, respectively) follicles, and the 10 ng/mL hrG-CSF medium (45.7%) follicle was significantly (P < 0.05) higher than in all other groups. The total cell number in blastocysts from the 10 ng/mL hrG-CSF medium (106.5) follicles was significantly (P < 0.05) increased compared to 0, 10, 100 ng/mL hrG-CSF small (55.0, 73.7 and 59.5, respectively) follicles and 0, 100 ng/mL hrG-CSF-treated medium (82.5 and 93.5, respectively) follicles. After IVF, the blastocysts stage was significantly (P < 0.05) increased in 10 ng/mL hrG-CSF-treated medium (36.4%) follicles. Fertilization efficiency was significantly high in 100 ng/mL of small (29.1%) and 10 ng/mL of medium (44.0%) follicles. We also examined the Bcl2 and ERK2 transcript levels and found that they were significantly higher in the small and medium follicle treatment groups. In conclusion, these results indicate that hrG-CSF improve the viability of porcine embryos. Copyright © 2015 Elsevier Inc. All rights reserved.
    Theriogenology 06/2015; 84(7). DOI:10.1016/j.theriogenology.2015.06.008 · 1.80 Impact Factor
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    ABSTRACT: Chamaecyparis obtusa has been traditionally used as an antibiotic agent and in cosmetics for the prevention of microorganism infection and skin troubles. Atopic dermatitis (AD) is a chronic inflammatory skin disease that encompasses immunologic responses, susceptibility factors and compromised skin-barrier function. Use of plant medicines in therapeutic treatment of AD has recently been suggested as an alternative therapeutic option. The present study examined the effect of elemol, an active component of Chamaecyparis obtusa, on AD using in vivo and in vitro models. RBL-2H3 cells were stimulated with concanavalin A and dinitrophenyl human serum albumin, and atopic dermatitis was induced in BALB/c mice by topical application of 2,4-dinitrochlorobenzene (DNCB) prior to elemol treatment. The mRNA expression was evaluated by reverse transcription quantitative polymerase chain reaction, and the levels of β-hexosaminidase and serum immunoglobulin E (IgE) were examined by ELISA. Histological changes were also performed by microscopy. Elemol attenuated the onset of AD-like skin lesions, reduced serum IgE levels and decreased mast cell infiltration into the dermis and hypodermis. In addition, elemol downregulated the transcriptional expression of several pro-inflammatory cytokines, including TNF-α, IL-1β, IL-6 and IκBα, in the skin of the DNCB‑induced animal models of AD. In the RBL-2H3 mast cell line, elemol significantly inhibited the mRNA expression of IL-4 and IL-13, and further attenuated the release of β-hexosaminidase from mast cells. Histological examination revealed that elemol significantly ameliorated the DNCB-induced dermal destruction in mice. The results of the present study suggested that elemol may have therapeutic potential in the treatment of AD due to its immunosuppressive effects.
    International Journal of Molecular Medicine 05/2015; 36(2). DOI:10.3892/ijmm.2015.2228 · 2.09 Impact Factor
  • Changhwan Ahn · Beum-Soo An · Eui-Bae Jeung ·
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    ABSTRACT: Calcium homeostasis refers to the regulation of calcium ion concentration in the body. This concentration is tightly controlled by a stabilizing system consisting of calcium channels and calcium buffering proteins. Calcium homeostasis is crucial for cell survival. Various forms of cell death (e.g., necrosis and apoptosis) also share calcium signaling pathways and molecular effectors. Calcium acts as not only a ubiquitous second messenger involved in apoptosis along with various cell death inducers but also a regulator for the synthesis of enzymes/hormones such as insulin. We hypothesized that streptozotocin disrupts calcium homeostasis and the altered intracellular calcium levels may induce cell death. After streptozotocin administration, blood glucose level was increased while insulin levels decreased. The expression of insulin response markers also decreased relative to the vehicle group. L-type voltage-gated calcium channels expression and sarcoplasmic reticulum Ca(2+) ATPase were increased by streptozotocin. Calcium buffering protein calbindin-D9k and calmodulin family members were also increased. The expression of genes involved in transporting calcium ions to the endoplasmic reticulum (ER) was decrease while the expression of those affecting the removal of calcium from the ER was increased. Depletion of calcium from the ER leads to ER-stress and can induce apoptosis. In the streptozotocin-treatment group, apoptosis markers were increased. Taken together, these results imply that the disruption of calcium homeostasis by streptozotocin induces ER-stress and leads to the apoptosis of pancreatic cells. Additionally, findings from this study suggest that imbalances in calcium homeostasis could promote pancreatic beta cell death and result in type I diabetes. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
    Molecular and Cellular Endocrinology 05/2015; 412. DOI:10.1016/j.mce.2015.05.017 · 4.41 Impact Factor
  • Changhwan Ahn · Hyun Yang · Dongoh Lee · Beum-soo An · Eui-Bae Jeung ·
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    ABSTRACT: Tight junctions (TJs) form continuous intercellular contacts controlling the paracellular transportation across the cell-to-cell junction. TJ components include the peripheral protein zonula occludens-1 (ZO-1), junctional adhesion molecules (JAMs), and integral proteins such as occludin and claudins. Among the junction proteins, claudins play a major role in regulation of paracellular electrolyte transportation. This study explores the expression and distribution of tight junctions and their regulation during pregnancy. To study the regulation of claudin family, we examined expression of mouse placental tight junction proteins, including Claudin-1 to -24, with real-time PCR and western blotting and distribution of tight junction proteins with immunohistochemistry. Pregnant C57/BL6 mice were used in this study. The pregnant mice were divided into three groups depending on pregnant day (on days 12, 16, and 20 of gestation). Regarding the transcription levels, claudin-1, claudin-2, claudin-4, and claudin-5 expression levels were relatively high compared to other claudin family in all periods of pregnancy. Claudin-4 and 5 expressions, which reduce ion permeability, were increased over a period of time. However, claudin-2 expression, that is the responsive protein for a decrease in paracellular conductance, was decreased. Following this modulation of expression during mid-term pregnancy, we identified endogenous hormonal modulation of claudin family using estrogen receptor antagonist ICI 182,780 and progesterone receptor antagonist RU-486. After administration of ICI and RU-486, expression of claudin-4 mRNA and protein was increased. In addition, immunohistochemistry was performed to identify their localization for inferring permeability in placenta. Due to the function of claudins as effectors of ion transport at the end of regulatory pathways, they must be transducing proteins that modulate the function of claudins and thus link the physiologic inputs to the final effectors. This study will provide the claudin expressions and their localization in the mouse placenta, and their regulation by endogenous hormones. Taken together, the results of this study may contribute to assuming the roles and regulatory mechanism of these tight junction genes regarding maternal-fetal ion transportation in the placenta. Copyright © 2015. Published by Elsevier Inc.
    Steroids 05/2015; 100. DOI:10.1016/j.steroids.2015.05.001 · 2.64 Impact Factor
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    Ji-Hye Han · Hye-Mi Kim · Deog-Gyu Seo · Gene Lee · Eui-Bae Jeung · Frank H Yu ·
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    ABSTRACT: Salivary fluid formation is primarily driven by Ca(2+)-activated, apical efflux of chloride into the lumen of the salivary acinus. The anoctamin1 protein is an anion channel with properties resembling the endogenous calcium-activated chloride channels. In order to better understand the role of anoctamin proteins in salivary exocrine secretion, the expression of the ten members of the anoctamin gene family in the mouse submandibular gland was studied. Total RNA extracted from mouse submandibular salivary glands was reverse transcribed using primer pairs to amplify the full-length coding regions of each anoctamin gene and was subcloned into plasmid vectors for DNA sequencing. Alternative splice variants were also screened by polymerase chain reaction using primer pairs that amplified six overlapping regions of the complementary DNA of each anoctamin gene, spanning multiple exons. Multiple anoctamin transcripts were found in the mouse submandibular salivary gland, including full-length transcripts of anoctamin1, anoctamin3, anoctamin4, anoctamin5, anoctamin6, anoctamin9, and anoctamin10. Exon-skipping splicing in the N-terminal exons of the anoctamins1, anoctamin5, and anoctamin6 genes resulted in multiple alternative splice variants. No expression of anoctamin2, anoctamin7, or anoctamin8 was found. The predominant anoctamin transcript expressed in the mouse submandibular gland is anoctamin1ac. The chloride channel protein produced by anoctamin1ac is likely responsible for the Ca(2+)-activated chloride efflux, which is the rate-limiting step in salivary exocrine secretion.
    Journal of periodontal & implant science 04/2015; 45(2):69-75. DOI:10.5051/jpis.2015.45.2.69 · 1.15 Impact Factor
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    ABSTRACT: Interferon α (IFN‑α) is a cytokine, produced predominantly in immune cells in response to pathogens, which interferes with viral replication in host cells. Another cytokine hormone, erythropoietin (EPO), is synthesized in interstitial fibroblasts of the kidney and acts as a stimulator for the production of red blood cells. Importantly, the two cytokines have been used in the treatment of certain hematological malignancies, including renal anemia. In the production of recombinant proteins, a transgenic expression system in bovine species is an efficient strategy for pharmaceutical production. In the present study, recombinant constructs capable of producing recombinant human IFN‑α and EPO proteins were established and were generated containing the mammary gland‑specific αS1‑casein promoter region (between ‑175 and +796 nt), as this promoter was revealed to have the highest level of activity in a previous promoter study. In order to minimize developmental toxicity by constitutive exogenous expression, a doxycycline (dox)‑inducible system was introduced to the IFN‑α/EPO‑expressing constructs. Therefore, a unitary tetracycline (tet)‑on the IFN‑α/EPO vector was established, which combined a tet‑on activator cassette controlled by the αS1‑casein promoter, with a responder cassette encoding the IFN‑α/EPO gene, controlled by the tetracycline response element (TRE) promoter. In these systems, the tet‑controlled transactivator is affected by mammary gland‑specific αS1‑casein promoter, and binding of the transcriptional activator to the TRE results in transcription of the downstream IFN‑α/EPO genes in the presence of dox. To assess this, the unitary tet‑on IFN‑α/EPO vector was introduced into a bovine mammary gland cell line (MAC‑T), and the cells were then treated with 0.1‑1 µg/ml dox. A marked increase was observed in the expression levels of IFN‑α/EPO. In addition, bovine transgenic fibroblasts containing a mammary gland‑specific and dox‑inducible IFN‑α/EPO construct were generated. These transgenic fibroblasts may provide a source for somatic cell nuclear transfer for the generation of transgenic cattle producing recombinant human IFN‑α/EPO protein during lactation.
    Molecular Medicine Reports 03/2015; 12(1). DOI:10.3892/mmr.2015.3483 · 1.55 Impact Factor
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    ABSTRACT: Aromatherapy has been suggested as an alternative therapeutic method for the treatment of atopic dermatitis (AD), eczema and other skin diseases. In the current study, the anti‑atopic properties of the volatile organic compounds of Chamaecyparis obtusa (VOCCo) were examined to determine whether they are amenable for use as a pharmaceutical candidate. The alterations in histological features, serum IgE levels and mast cell infiltration following exposure to VOCCo were determined in a 2,4-dinitrochlorobenzene (DNCB)-induced AD-like mouse model. The results of these experiments demonstrated that VOCCo inhibited the development of AD‑like skin lesions by reducing the serum IgE level and mast cell infiltration into the dermal and subcutaneous layers. This was supported by screening of immune cytokine mRNAs, including interleukin (IL)‑1β and IL‑6 from the skin of DNCB‑treated mice. The expression of IL‑1β and IL‑6 in the skin lesions of mice was dose-dependently inhibited by treatment with VOCCo. Furthermore, treatment with VOCCo resulted in the recovery of histopathological features in AD-like skin lesions. These results suggest that VOCCo may have therapeutic and preventive effects for the development of AD.
    Molecular Medicine Reports 03/2015; 12(1). DOI:10.3892/mmr.2015.3431 · 1.55 Impact Factor
  • Eui-Ju Hong · Yeoul Choi · Hyun Yang · Hee Young Kang · Changhwan Ahn · Eui-Bae Jeung ·
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    ABSTRACT: Embryonic stem (ES) cells have the capacity for self-renewal and differentiation into three germ layers following formation of embryonic bodies (EB). To investigate toxicity of pharmaceutical compounds, five toxic chemicals, indomethacin, dexamethasone, hydroxyurea, 5-fluorouracil, and cytosine arabinoside were applied in mouse ES cells during formation of EBs. Using microscopic evaluation, the size of EBs was reduced in a dose-dependent manner by treatment with pharmaceutical chemicals. While apoptosis-related proteins, cleaved caspase-3 and PARP, were decreased in compound-exposed EBs, necrosis-related protein (Hmgb1) was present in culture media of EBs, indicating that detection of Hmgb1 can result in activation of necrosis by pharmaceutical compounds. While pharmaceutical compounds impaired the differentiation of mES cells linked with spontaneous apoptotic cell death, it was determined that cytotoxic cell damage is necrosis-dependent in mES cells. In addition, an apoptotic transcript (Noxa mRNA) in toxicant-exposed EBs was decreased in parallel with apoptosis-related proteins. Following impairment of apoptosis, differentiation-related markers including un-differentiation (Sox2), endoderm (Hnf4), mesoderm (Bmp4), and ectoderm (Pax6) also fluctuated by treatment with pharmaceutical compounds. Taken together, the data imply that exposure to pharmaceutical compounds results in increased cell death hindering the spontaneous apoptosis of cells to undergo differentiation. Using both characteristics of ES cells like self-renewal or cellular pluripotency and potentials of ES cells for evaluation in toxicity of various compounds, the current study was conducted for establishment of a novel drug screening system beyond hidden virtues of the well-known chemicals. Copyright © 2014 Elsevier B.V. All rights reserved.
    Environmental Toxicology and Pharmacology 12/2014; 39(1):327-338. DOI:10.1016/j.etap.2014.12.003 · 2.08 Impact Factor
  • Hyun Yang · Changhwan Ahn · Eui-Bae Jeung ·
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    ABSTRACT: Preeclampsia is a pregnancy-specific disease characterized by concurrent development of hypertension, proteinuria, and oxidative stress in the placenta. Preeclampsia-like genetic models were also developed by modification of preeclampsia-related genes, such as catechol-O-methyltranferase (COMT). In this study, we induced COMT inhibition in mice during pregnancy in order to reproduce physiological conditions associated with preeclampsia. Expression of the gene known as hypoxia biomarker, HIF-1α, was highly induced in the placenta of this model. The over-expression of HIF-1α demonstrates that our experimental conditions were similar to those of preeclampsia. We measured the expression of several calcium transport genes (CTGs; TRPV5, TRPV6, PMCA1 and CaBP-9k) in the placenta, duodenum and kidney after COMT inhibition on gestation day 17.5 (GD 17.5). In addition, we evaluated the calcium transporters in the kidney, duodenum of non-pregnant female mice. Placental TRPV5, TRPV6 and PMCA1 expressions were down-regulated by COMT inhibitor (ro41-0960). In addition, the reduced PMCA1 expression in the placenta was reversed by calcium supplementation. Duodenal expressions of TRPV5, TRPV6, and PMCA1 were decreased in COMT-inhibited mice, and recovered slightly after calcium supplementation. Renal expression of TRPV5, TRPV6, and PMCA1 was also decreased by COMT inhibition, while it was reversed by calcium supplementation to the level of control. Duodenal- and renal calcium transporting genes, TRPV5, TPRV6, PMCA1 and CaBP-9k, were down-regulated by COMT treatment in female mice. Taken together, these results indicate that physiological changes observed in COMT inhibition were similar to symptoms of preeclampsia, which may be related to disturbance of calcium metabolism during pregnancy. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
    Molecular and Cellular Endocrinology 12/2014; 401(C). DOI:10.1016/j.mce.2014.11.020 · 4.41 Impact Factor
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    Han Sung Kim · Seung-Il Choi · Eui-Bae Jeung · Yeong-Min Yoo ·
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    ABSTRACT: Cyclosporine A (CsA) is a powerful immunosuppressive drug with side effects including the development of chronic nephrotoxicity. In this study, we investigated CsA treatment induced apoptotic and autophagic cell death in pituitary GH3 cells. CsA treatment (0.1 to 10 µM) decreased survival of GH3 cells in a dose-dependent manner. Cell viability decreased significantly with increasing CsA concentrations largely due to an increase in apoptosis, while cell death rates due to autophagy altered only slightly. Several molecular and morphological features correlated with cell death through these distinct pathways. At concentrations ranging from 1.0 to 10 µM, CsA induced a dose-dependent increase in expression of the autophagy markers LC3-I and LC3-II. Immunofluorescence staining revealed markedly increased levels of both LC3 and lysosomal-associated membrane protein 2 (Lamp2), indicating increases in autophagosomes. At the same CsA doses, apoptotic cell death was apparent as indicated by nuclear and DNA fragmentation and increased p53 expression. In apoptotic or autophagic cells, p-ERK levels were highest at 1.0 µM CsA compared to control or other doses. In contrast, Bax levels in both types of cell death were increased in a dose-dependent manner, while Bcl-2 levels showed dose-dependent augmentation in autophagy and were decreased in apoptosis. Manganese superoxide dismutase (Mn-SOD) showed a similar dose-dependent reduction in cells undergoing apoptosis, while levels of the intracellular calcium ion exchange maker calbindin-D9k were decreased in apoptosis (1.0 to 5 µM CsA), but unchanged in autophagy. In conclusion, these results suggest that CsA induction of apoptotic or autophagic cell death in rat pituitary GH3 cells depends on the relative expression of factors and correlates with Bcl-2 and Mn-SOD levels.
    PLoS ONE 10/2014; 9(10):e108981. DOI:10.1371/journal.pone.0108981 · 3.23 Impact Factor
  • Ji-Sun Lee · Eui-Bae Jeung ·

    09/2014; DOI:10.1530/repabs.1.P279
  • Hyun Yang · Young-Kwon Choi · Eui-Bae Jeung ·

    09/2014; DOI:10.1530/repabs.1.P267

Publication Stats

4k Citations
506.39 Total Impact Points


  • 2002-2015
    • Chungbuk National University
      • College of Veterinary Medicine
      Chinsen, Chungcheongbuk-do, South Korea
  • 2012
    • University of Michigan
      • Life Sciences Institute
      Ann Arbor, MI, United States