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Search Results: 1 - 10 of 41540 matches for " Sung Eun Hong3 "
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Cyclosporine A and bromocriptine attenuate cell death mediated by intracellular calcium mobilization
In Ki Kim1*, So Jung Park1, Jhang Ho Park1, Seung-Ho Lee2, Sung Eun Hong3 & John C. Reed3
BMB Reports , 2012,
Abstract: To identify the novel inhibitors of endoplasmic reticulumstress-induced cell death, we performed a high throughput assaywith a chemical library containing a total of 3280 bioactive smallmolecules. Cyclosporine A and bromocriptine were identified aspotent inhibitors of thapsigargiin-induced cell death (cut-off at4σ standard score) . However, U74389G, the potent inhibitor oflipid peroxidation had lower activity in inhibiting cell death. Theinhibition effect of cyclosporine A and bromocriptine wasspecific for only thapsigargin-induced cell death. The mechanismof inhibition by these compounds was identified as modificationof the expression of glucose regulated protein-78 (GRP-78/Bip)and inhibition of phosphorylation of p38 mitogen activatedprotein kinase (MAPK). However, these compounds did notinhibit the same events triggered by tunicamycin, which was inagreement with the cell survival data. We suggest that theinduction of protective unfolded protein response by thesecompounds confers resistance to cell death. In summary, weidentified compounds that may provide insights on cell deathmechanisms stimulated by ER stress.
Clinical Implications of Adipocytokines and Newly Emerging Metabolic Factors with Relation to Insulin Resistance and Cardiovascular Health
Sung Hee Choi,Eun Shil Hong
Frontiers in Endocrinology , 2013, DOI: 10.3389/fendo.2013.00097
Abstract: Adipose tissue is known to secrete hormones actively and produces many biologically active proteins called adipocytokines. Typically, obesity is followed by low-grade inflammation, which is characterized by increased circulating levels of pro-inflammatory cytokines. Macrophages play a role in the inflammatory process by secreting many cytokines such as tumor necrosis factor alpha, interleukin-6, resistin, and retinol binding protein-4. These cytokines and chemokines participate in low-grade pro-inflammatory processes leading to insulin resistance, metabolic impairment, and cardiovascular diseases. More metabolic regulators, such as fibroblast growth factor (FGF)21, FGF19, FGF1, vaspin, and visfatin have now been discovered but their exact roles in human diseases are still unclear. This review focuses on recent research regarding the role of adipokines and new metabolic factors in metabolic derangement or cardiovascular disease.
Biotransformation of endosulfan by the tiger worm, Eisenia fetida  [PDF]
Byeoung-Soo Park, Jae-Hong Yoo, Jeong-Han Kim, Sung-Eun Lee, Jang-Eok Kim
Journal of Agricultural Chemistry and Environment (JACEN) , 2012, DOI: 10.4236/jacen.2012.11004
Abstract: This study assesses the role of the earthworm, Eisenia fetida, in the breakdown of endosulfan in a soil environment. Two strains of E. fetida were used in this study to assess the effect of salinity on toxicity and metabolism of endosulfan in these earthworms. One strain of E. fetida (R) was reared in high salinity soil (over 2.0 dS/m of electric conductivity) from Shiwha lake, Korea. A control strain (W) was reared in pig manure compost. Acute toxicity of endosulfan was lower in the R strain when endosulfan was injected. In vitro metabolic studies of endosulfan based on microsomal preparations showed that both strains produced two major metabolites, endosulfan sulfate and endosulfan diol. The production rate of endodulfan sulfate was not significantly different between the strains, while endosulfan diol production was significantly different. In vivo metabolism studies showed only one primary metabolite, endosulfan sulfate, was produced by both strains. HPLC-MS/MS analysis showed annetocin was the indicative protein newly expressed in the R strain in relation to salinity exposure. These findings suggest salinity may induce hydrolyzing enzymes to produce endosulfan diol from endosulfan.
Potential role and mechanism of IFN-gamma inducible protein-10 on receptor activator of nuclear factor kappa-B ligand (RANKL) expression in rheumatoid arthritis
Eun Lee, MiRan Seo, Yong-Sung Juhnn, Jeong Kim, Yoo Hong, Yun Lee, Eun Lee, Yeong Song
Arthritis Research & Therapy , 2011, DOI: 10.1186/ar3385
Abstract: Synoviocytes derived from RA patients were kept in culture for 24 hours in the presence or absence of TNF-α. CXCL10 expression was measured by reverse transcriptase polymerase chain reaction (RT-PCR) of cultured synoviocytes. Expression of RANKL was measured by RT-PCR and western blot in cultured synoviocytes with or without CXCL10 and also measured in Jurkat/Hut 78 T cells and CD4+ T cells in the presence of CXCL10 or dexamethasone. CXCL10 induced RANKL expression in Jurkat T cells was tested upon the pertussis toxin (PTX), an inhibitor of Gi subunit of G protein coupled receptor (GPCR). The synthetic siRNA for Gαi2 was used to knock down gene expression of respective proteins.CXCL10 expression in RA synoviocytes was increased by TNF-α. CXCL10 slightly increased RANKL expression in RA synoviocytes, but markedly increased RANKL expression in Jurkat/Hut 78 T cell or CD4+ T cell. CXCL10 augmented the expression of RANKL by 62.6%, and PTX inhibited both basal level of RANKL (from 37.4 ± 16.0 to 18.9 ± 13.0%) and CXCL10-induced RANKL expression in Jurkat T cells (from 100% to 48.6 ± 27.3%). Knock down of Gαi2 by siRNA transfection, which suppressed the basal level of RANKL (from 61.8 ± 17.9% to 31.1 ± 15.9%) and CXCL10-induced RANKL expression (from 100% to 53.1 ± 27.1%) in Jurkat T cells, is consistent with PTX, which inhibited RANKL expression.CXCL10 increased RANKL expression in CD4+ T cells and it was mediated by Gαi subunits of CXCR3. These results indicate that CXCL10 may have a potential role in osteoclastogenesis of RA synovial tissue and subsequent joint erosion.Interferon-gamma (IFN-γ)-inducible protein 10 (CXCL10, also called IP-10) was initially identified as a chemokine that is induced by IFN-γ and secreted by various cell types, such as monocytes, neutrophils, endothelial cells, keratinocytes, fibroblasts, mesenchymal cells, dendritic cells, and astrocytes [1]. CXCL10 is a 10-kDa protein and is functionally categorized as an 'inflammatory' chemokine. Moreo
Molecular cloning and expression analysis of peptidase genes in the fish-pathogenic scuticociliate Miamiensis avidus
Jung Soo Seo, Eun Ji Jeon, Sung Hee Jung, Myoung Ae Park, Jin Woo Kim, Ki Hong Kim, Sung Ho Woo, Eun Hye Lee
BMC Veterinary Research , 2013, DOI: 10.1186/1746-6148-9-10
Abstract: The 17 genes encoding peptidases, including seven cathepsin-like cysteine peptidases, four serine carboxypeptidases, a eukaryotic aspartyl protease family protein, an ATP-dependent metalloprotease FtsH family protein, three leishmanolysin family proteins and a peptidase family M49 protein were identified from a Miamiensis avidus cDNA library by BLAST X search. Expression of genes encoding two cysteine peptidases, three leishmanolysin-like peptidases and a peptidase family M49 protein was up-regulated in the cell-fed ciliates compared to the starved ciliates. Especially, one cysteine peptidase (MaPro 4) and one leishmanolysin-like peptidase (MaPro 14) were transcribed more than 100-folds in the cell-fed ciliates.The genetic information and transcriptional characteristics of the peptidases in the present results would be helpful to elucidate the role of peptidases in the invasion of scuticociliates into their hosts.
Diosgenin Induces Apoptosis in HepG2 Cells through Generation of Reactive Oxygen Species and Mitochondrial Pathway
Dae Sung Kim,Byoung Kook Jeon,Young Eun Lee,Won Hong Woo,Yeun Ja Mun
Evidence-Based Complementary and Alternative Medicine , 2012, DOI: 10.1155/2012/981675
Abstract: Diosgenin, a naturally occurring steroid saponin found abundantly in legumes and yams, is a precursor of various synthetic steroidal drugs. Diosgenin is studied for the mechanism of its action in apoptotic pathway in human hepatocellular carcinoma cells. Based on DAPI staining, diosgenin-treated cells manifested nuclear shrinkage, condensation, and fragmentation. Treatment of HepG2 cells with 40 M diosgenin resulted in activation of the caspase-3, -8, -9 and cleavage of poly-ADP-ribose polymerase (PARP) and the release of cytochrome c. In the upstream, diosgenin increased the expression of Bax, decreased the expression of Bid and Bcl-2, and augmented the Bax/Bcl-2 ratio. Diosgenin-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of JNK, p38 MAPK and apoptosis signal-regulating kinase (ASK)-1, as well as generation of the ROS. NAC administration, a scavenger of ROS, reversed diosgene-induced cell death. These results suggest that diosgenin-induced apoptosis in HepG2 cells through Bcl-2 protein family-mediated mitochndria/caspase-3-dependent pathway. Also, diosgenin strongly generated ROS and this oxidative stress might induce apoptosis through activation of ASK1, which are critical upstream signals for JNK/p38 MAPK activation in HepG2 cancer cells.
Inhibition of glutamate dehydrogenase and insulin secretion by KHG26377 does not involve ADP-ribosylation by SIRT4 or deacetylation by SIRT3
Eun-A Kim1,#, Seung-Ju Yang2,#, Soo Young Choi3, Woo Je Lee4,* & Sung-Woo Cho1,*
BMB Reports , 2012,
Abstract: We investigated the mechanisms involved in KHG26377 regulationof glutamate dehydrogenase (GDH) activity, focusing onthe roles of SIRT4 and SIRT3. Intraperitoneal injection of micewith KHG26377 reduced GDH activity with concomitant repressionof glucose-induced insulin secretion. Consistent withtheir known functions, SIRT4 ribosylated GDH and reduced itsactivity, and SIRT3 deacetylated GDH, increasing its activity.However, KHG26377 did not affect SIRT4-mediated ADP-ribosylation/inhibition or SIRT3-mediated deacetylation/activationof GDH. KHG26377 had no effect on SIRT4 protein levels,and did not alter total GDH, acetylated GDH, or SIRT3 proteinlevels in pancreatic mitochondrial lysates. These results suggestthat the mechanism by which KHG26377 inhibits GDHactivity and insulin secretion does not involve ADP-ribosylationof GDH by SIRT4 or deacetylation of GDH by SIRT3.
Induction of IL-10-Producing CD1dhighCD5+ Regulatory B Cells following Babesia microti-Infection
Young-Il Jeong, Sung-Hee Hong, Shin-Hyeong Cho, Won-Ja Lee, Sang-Eun Lee
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0046553
Abstract: Background Understanding the induction of immune regulatory cells upon helminth infection is important for understanding the control of autoimmunity and allergic inflammation in helminth infection. Babesia microti, an intraerythrocytic protozoan of the genus Babesia, is a major cause of the emerging human disease babesiosis, an asymptomatic malaria-like disease. We examined the influence of acute B. microti infection on the development of regulatory B cells together with regulatory T cells. Principal Findings Our data demonstrate that B cells stimulated in vitro with B. microti produce interleukin (IL)-10. This cytokine is also secreted by B cells isolated from B. microti-infected mice in response to lipopolysaccharide stimulation. In addition, high levels of IL-10 were detected in the serum of mice after infection with B. microti. The frequency of IL-10-producing CD1dhighCD5+ regulatory B cells (Bregs) and CD4+CD25+FoxP3+ T cells increased during the course of B. microti infection. Furthermore, adoptive transfer of IL-10-producing B cells induced by B. microti infection led to increased susceptibility of recipient mice to infection with B. microti. In contrast, experiments with B cell-deficient (μMT) mice demonstrated that lack of B cells enhances susceptibility to B. microti infection. Conclusions This study is the first demonstration of the expansion of Bregs following infection by an intraerythrocytic protozoan parasite. These data suggest that B. microti infection in mice provides an excellent model for studying Breg-mediated immune responses and begins to elucidate the mechanism by which helminth infection regulates autoimmunity and allergic inflammation.
Intravenous Vitamin C administration reduces fatigue in office workers: a double-blind randomized controlled trial
Sang-Yeon Suh, Woo Bae, Hong-Yup Ahn, Sung-Eun Choi, Gyou-Chul Jung, Chang Yeom
Nutrition Journal , 2012, DOI: 10.1186/1475-2891-11-7
Abstract: We evaluated the effect of intravenous vitamin C on fatigue in office workers. A group of 141 healthy volunteers, aged 20 to 49 years participated in this randomized, double-blind, controlled clinical trial. The trial group received 10 grams of vitamin C with normal saline intravenously, while the placebo group received normal saline only. Since vitamin C is a well-known antioxidant, oxidative stress was measured. Fatigue score, oxidative stress, and plasma vitamin C levels were measured before intervention, and again two hours and one day after intervention. Adverse events were monitored.The fatigue scores measured at two hours after intervention and one day after intervention were significantly different between the two groups (p = 0.004); fatigue scores decreased in the vitamin C group after two hours and remained lower for one day. Trial also led to higher plasma vitamin C levels and lower oxidative stress compared to the placebo group (p < 0.001, p < 0.001, respectively). When data analysis was refined by dividing each group into high-baseline and low-baseline subgroups, it was observed that fatigue was reduced in the lower baseline vitamin C level group after two hours and after one day (p = 0.004). The same did not hold for the higher baseline group (p = 0.206).Thus, intravenous vitamin C reduced fatigue at two hours, and the effect persisted for one day. There were no significant differences in adverse events between two groups. High dose intravenous vitamin C proved to be safe and effective against fatigue in this study.The clinical trial registration of this trial is http://ClinicalTrials.gov webciteNCT00633581.Fatigue is one of the most common complaints in daily life, and the prevalence of fatigue is high in full-time workers. Previous studies have shown that 27% of adults, who were weekly assessed, experienced fatigue [1], and 32.5% of patients who visited primary care clinics complained of fatigue [2]. Oxidative stress is thought to underlie fatigue to
Crude Extracts of Caenorhabditis elegans Suppress Airway Inflammation in a Murine Model of Allergic Asthma
Sung Eun Kim, Jae-Hwan Kim, Byung-Hoon Min, Young Mee Bae, Sung-Tae Hong, Min-Ho Choi
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035447
Abstract: Epidemiological studies suggest an inverse relationship between helminth infections and allergic disease, and several helminth-derived products have been shown to suppress allergic responses in animals. This study was undertaken to evaluate the effect of a crude extract of Caenorhabditis elegans on allergic airway inflammation in a murine model of asthma. Allergic airway inflammation was induced in BALB/c mice by sensitization with ovalbumin. The effect of the C. elegans crude extract on the development of asthma and on established asthma was evaluated by analyzing airway hyperresponsiveness, serum antibody titers, lung histology and cell counts and cytokine levels in the bronchoalveolar lavage fluid. The role of IFN-γ in the suppression of asthma by the C. elegans crude extract was investigated in IFN-γ knockout and wild-type mice. When mice were sensitized with ovalbumin together with the crude extract of C. elegans, cellular infiltration into the lung was dramatically reduced in comparison with the ovalbumin-treated group. Treatment of mice with the C. elegans crude extract significantly decreased methacholine-induced airway hyperresponsiveness and the total cell counts and levels of IL-4, IL-5 and IL-13 in the bronchoalveolar lavage fluid but increased the levels of IFN-γ and IL-12. Sensitization with the C. elegans crude extract significantly diminished the IgE and IgG1 responses but provoked elevated IgG2a levels. However, the suppressive effect of the C. elegans crude extract was abolished in IFN-γ knockout mice, and the Th2 responses in these mice were as strong as those in wild-type mice sensitized with ovalbumin. The crude extract of C. elegans also suppressed the airway inflammation associated with established asthma. This study provides new insights into immune modulation by the C. elegans crude extract, which suppressed airway inflammation in mice not only during the development of asthma but also after its establishment by skewing allergen-induced Th2 responses to Th1 responses.
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