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Search Results: 1 - 10 of 28324 matches for " Sung-Hee Lee "
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Role of DUOX in gut inflammation: Lessons from Drosophila model of gut-microbiota interactions.
Won-Jae Lee,Sung-Hee Kim
Frontiers in Cellular and Infection Microbiology , 2013, DOI: 10.3389/fcimb.2013.00116
Abstract: It is well known that certain bacterial species can colonize the gut epithelium and induce inflammation in the mucosa, whereas other species are either benign or beneficial to the host. Deregulation of the gut-microbe interactions may lead to a pathogenic condition in the host, such as chronic inflammation, tissue injuries, and even cancer. However, our current understanding of the molecular mechanisms that underlie gut-microbe homeostasis and pathogenesis remains limited. Recent studies have used Drosophila as a genetic model to provide novel insights into the causes and consequences of bacterial-induced colitis in the intestinal mucosa. The present review discusses the interactions that occur between gut-associated bacteria and host gut immunity, particularly the bacterial-induced intestinal dual oxidase (DUOX) system. Several lines of evidence showed that the bacterial-modulated DUOX system is involved in microbial clearance, intestinal epithelial cell renewal, redox-dependent modulation of signaling pathways, cross-linking of biomolecules, and discrimination between symbionts and pathogens. Further genetic studies on the Drosophila DUOX system and on gut-associated bacteria with a distinct ability to activate DUOX may provide critical information related to the homeostatic inflammation as well as etiology of chronic inflammatory diseases, which will enhance our understanding on the mucosal inflammatory diseases frequently observed in the microbe-contacting epithelia of humans.
Metabolic alteration of urinary steroids in pre- and post-menopausal women, and men with papillary thyroid carcinoma
Man Choi, Ju-Yeon Moon, Sung-Hee Cho, Bong Chung, Eun Lee
BMC Cancer , 2011, DOI: 10.1186/1471-2407-11-342
Abstract: Quantitative steroid profiling combined with gas chromatography-mass spectrometry was used to measure the urinary concentrations of 84 steroids in both pre- (n = 21, age: 36.95 ± 7.19 yr) and post-menopausal female (n = 19, age: 52.79 ± 7.66 yr), and male (n = 16, age: 41.88 ± 8.48 yr) patients with PTC. After comparing the quantitative data of the patients with their corresponding controls (pre-menopause women: n = 24, age: 33.21 ± 10.48 yr, post-menopause women: n = 16, age: 49.67 ± 8.94 yr, male: n = 20, age: 42.75 ± 4.22 yr), the levels of steroids in the patients were normalized to the mean concentration of the controls to exclude gender and menopausal variations.Many urinary steroids were up-regulated in all PTC patients compared to the controls. Among them, the levels of three active androgens, androstenedione, androstenediol and 16α-hydroxy DHEA, were significantly higher in the pre-menopausal women and men with PTC. The corticoid levels were increased slightly in the PTC men, while progestins were not altered in the post-menopausal PTC women. Estrogens were up-regulated in all PTC patients but 2-hydroxyestrone and 2-hydroxy-17β-estradiol were remarkably changed in both pre-menopausal women and men with PTC. For both menopausal and gender differences, the 2-hydroxylation, 4-hydroxylation, 2-methoxylation, and 4-methoxylation of estrogens and 16α-hydroxylation of DHEA were differentiated between pre- and post-menopausal PTC women (P < 0.001). In particular, the metabolic ratio of 2-hydroxyestrone to 2-hydroxy-17β-estradiol, which could reveal the enzyme activity of 17β-hydroxysteroid dehydrogenase, showed gender differences in PTC patients (P < 1 × 10-7).These results are expected be helpful for better understanding the pathogenic differences in PTC according to gender and menopausal conditions.Papillary thyroid carcinoma (PTC) is the commonest of all thyroid carcinomas and is well-differentiated. The incidence of PTC is three times higher in women than men [
Effect of collagen and collagen peptides from bluefin tuna abdominal skin on cancer cells  [PDF]
Sung-Hee Han, Yuki Uzawa, Tatsuya Moriyama, Yukio Kawamura
Health (Health) , 2011, DOI: 10.4236/health.2011.33024
Abstract: In the present study, we investigated the effect of collagen and collagen peptides from bluefin tuna abdominal skin on cancer cells. Collagens were extracted from bluefin tuna (Thunnus orientails) abdominal, mackerel, and carp skin. The calf and salmon collagen were used reagent grade as a standard samples. The main protein band pattern produced by SDS-PAGE of all collagen samples consisted of two chains and one chain. For collagen peptides samples, bluefin tuna ab-dominal skin collagen and salmon skin collagen were hydrolyzed by trypsin. Among samples, salmon, mackerel, carp collagen, and their collagen peptides did not significantly reduce relative cell growth. However, the bluefin tuna abdominal skin collagen dramatically reduced HepG2 and HeLa cell growth by over 50% relative in a concentration-dependent manner when added to cells seeded 96-well plates. This suggests the collagen adding time was mightily important for effect of the collagen.
Flexible Pavement Analysis Considering Temperature Profile and Anisotropy Behavior in Hot Mix Ashalt Layer  [PDF]
Joonho Choi, Youngguk Seo, Sung-Hee Kim, Samuel Beadles
Open Journal of Civil Engineering (OJCE) , 2011, DOI: 10.4236/ojce.2011.12002
Abstract: A three Dimensional finite element model (FEM) incorporating the anisotropic properties and temperature profile of hot mix asphalt (HMA) pavement was developed to predict the structural responses of HMA pavement subject to heavy loads typically encountered in the field. In this study, ABAQUS was adopted to model the stress and strain relationships within the pavement structure. The results of the model were verified using data collected from the Korean Highway Corporation Test Road (KHCTR). The results demonstrated that both the base course and surface course layers follow the anisotropic behavior and the incorporation of the temperature profile throughout the pavement has a substantial effect on the pavement response predictions that impact pavement design. The results also showed that the anisotropy level of HMA and base material can be reduced to as low as 80% and 15% as a result of repeated loading, respectively.
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.
Compound K, a metabolite of ginseng saponin, induces apoptosis via caspase-8-dependent pathway in HL-60 human leukemia cells
Sung-Hee Cho, Kyung-Sook Chung, Jung-Hye Choi, Dong-Hyun Kim, Kyung-Tae Lee
BMC Cancer , 2009, DOI: 10.1186/1471-2407-9-449
Abstract: We examined the effect of Compound K on the viabilities of various cancer cell lines using MTT assays. DAPI assay, Annexin V and PI double staining, Western blot assay and immunoprecipitation were used to determine the effect of Compound K on the induction of apoptosis.Compound K was found to inhibit the viability of HL-60 cells in a dose- and time-dependent manner with an IC50 of 14 μM. Moreover, this cell death had typical features of apoptosis, that is, DNA fragmentation, DNA ladder formation, and the externalization of Annexin V targeted phosphatidylserine residues in HL-60 cells. In addition, compound-K induced a series of intracellular events associated with both the mitochondrial- and death receptor-dependent apoptotic pathways, namely, (1) the activation of caspases-3, -8, and -9; (2) the loss of mitochondrial membrane potential; (3) the release of cytochrome c and Smac/DIABLO to the cytosol; (4) the translocation of Bid and Bax to mitochondria; and (5) the downregulations of Bcl-2 and Bcl-xL. Furthermore, a caspase-8 inhibitor completely abolished caspase-3 activation, Bid cleavage, and subsequent DNA fragmentation by Compound K. Interestingly, the activation of caspase-3 and -8 and DNA fragmentation were significantly prevented in the presence of cycloheximide, suggesting that Compound K-induced apoptosis is dependent on de novo protein synthesis.The results indicate that caspase-8 plays a key role in Compound K-stimulated apoptosis via the activation of caspase-3 directly or indirectly through Bid cleavage, cytochrome c release, and caspase-9 activation.Ginseng, the root and rhizomes of different Panax species (Araliaceae), is one of the most commonly used as traditional medicines in East Asia. Furthermore, the saponins of ginseng (ginsenosides) are its major active components and have been shown to possess anti-inflammatory, anti-tumor, and neuroprotective activities [1]. The pharmacological actions of these ginsenosides have been attributed to their bio
Loss of the Promyelocytic Leukemia Protein in Gastric Cancer: Implications for IP-10 Expression and Tumor-Infiltrating Lymphocytes
Hee Ja Kim, Dong Eun Song, Seul Ye Lim, Sung-Hee Lee, Jihee Lee Kang, Sun Jung Lee, Etty N. Benveniste, Youn-Hee Choi
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0026264
Abstract: Gastric cancer is one of the most common causes of cancer-related mortality worldwide. Expression of the tumor suppressor, promyelocytic leukemia (PML) protein, is reduced or abolished in gastric carcinomas, in association with an increased level of lymphatic invasion, development of higher pTNM staging, and unfavorable prognosis. Herein, we investigated the relationship between the extent of tumor-infiltrating lymphocytes and the status of PML protein expression in advanced gastric carcinoma. We observed higher numbers of infiltrating T-cells in gastric carcinoma tissues in which PML expression was reduced or abolished, compared to tissues positive for PML. The extent of T-cell migration toward culture supernatants obtained from interferon-gamma (IFN-γ-stimulated gastric carcinoma cell lines was additionally affected by expression of PML in vitro. Interferon-gamma-inducible protein 10 (IP-10/CXCL10) expression was increased in gastric carcinoma tissues displaying reduced PML levels. Moreover, both Pml knockout and knockdown cells displayed enhanced IP-10 mRNA and protein expression in the presence of IFN-γ. PML knockdown increased IFN-γ-mediated Signal Transducer and Activator of Transcription-1 (STAT-1) binding to the IP-10 promoter, resulting in elevated transcription of the IP-10 gene. Conversely, PML IV protein expression suppressed IP-10 promoter activation. Based on these results, we propose that loss of PML protein expression in gastric cancer cells contributes to increased IP-10 transcription via enhancement of STAT-1 activity, which, in turn, promotes lymphocyte trafficking within tumor regions.
SHP-2 Binds to Caveolin-1 and Regulates Src Activity via Competitive Inhibition of CSK in Response to H2O2 in Astrocytes
Ara Jo, Hyunju Park, Sung-Hee Lee, So-Hee Ahn, Hee Ja Kim, Eun-Mi Park, Youn-Hee Choi
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0091582
Abstract: Reactive oxygen species (ROS) regulate diverse cellular functions by triggering signal transduction events, such as Src and mitogen-activated protein (MAP) kinases. Here, we report the role of caveolin-1 and Src homology 2 domain-containing protein tyrosine phosphatase 2 (SHP-2) in H2O2-induced signaling pathway in brain astrocytes. H2O2-mediated oxidative stress induced phosphorylation of caveolin-1 and association between p-caveolin-1 and SHP-2. SHP-2 specifically bound to wild-type caveolin-1 similarly to c-Src tyrosine kinase (CSK), but not to phosphorylation-deficient mutant of caveolin-1 (Y14A), and interfered with complex formation between caveolin-1 and CSK. In the presence of CSK siRNA, binding between caveolin-1 and SHP-2 was enhanced by H2O2 treatment, which led to reduced Src phosphorylation at tyrosine (Tyr) 530 and enhanced Src phosphorylation at Tyr 419. In contrast, siRNA targeting of SHP-2 facilitated H2O2-mediated interaction between caveolin-1 and CSK and enhanced Src phosphorylation at Tyr 530, leading to subsequent decrease in Src downstream signaling, such as focal adhesion kinase (FAK) and extracellular signal-related kinase (ERK). Our results collectively indicate that SHP-2 alters Src kinase activity by interfering with the complex formation between CSK and phosphotyrosine caveolin-1 in the presence of H2O2, thus functions as a positive regulator in Src signaling under oxidative stress in brain astrocytes.
Characterizations of individual mouse red blood cells parasitized by Babesia microti using 3-D holographic microscopy
HyunJoo Park,Sung-Hee Hong,Kyoohyun Kim,Shin-Hyeong Cho,Won-Ja Lee,Youngchan Kim,Sang-Eun Lee,YongKeun Park
Physics , 2015,
Abstract: Babesia microti causes emergency human babesiosis. However, little is known about the alterations in B. microti invaded red blood cells (Bm-RBCs) at the individual cell level. Through quantitative phase imaging techniques based on laser interferometry, we present the simultaneous measurements of structural, chemical, and mechanical modifications in individual mouse Bm-RBCs. 3-D refractive index maps of individual RBCs and in situ parasite vacuoles are imaged, from which total contents and concentration of dry mass are also precisely quantified. In addition, we examine the dynamic membrane fluctuation of Bm-RBCs, which provide information on cell membrane deformability.
Curcumin Attenuates Acute Graft-versus-Host Disease Severity via In Vivo Regulations on Th1, Th17 and Regulatory T Cells
Min-Jung Park, Su-Jin Moon, Sung-Hee Lee, Eun-Ji Yang, Jun-Ki Min, Seok-Goo Cho, Chul-Woo Yang, Sung-Hwan Park, Ho-Youn Kim, Mi-La Cho
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0067171
Abstract: Background In this study we examined the in vivo and in vitro effects and mechanisms of action of curcumin on the development of acute graft-versus-host disease (GVHD) using a murine model. Methodology/Principal Findings Mixed lymphocyte reactions were used to determine the in vitro effects of curcumin. Treatment with curcumin attenuated alloreactive T cell proliferation and inhibited the production of interferon (IFN)-γ and interleukin (IL)-17. In a murine acute GVHD model, transplantation of curcumin-treated allogeneic splenocytes into irradiated recipient mice significantly reduced the clinical severity scores of acute GVHD manifested in the liver, skin, colon and lung as compared with animals receiving vehicle-treated splenocytes. c-Fos and c-Jun expression levels in the skin and intestine, which are major target organs, were analyzed using immunohistochemical staining. Expression of both proteins was reduced in epithelial tissues of skin and intestine from curcumin-treated GVHD animals. The IFN-γ-expressing CD4+ splenocytes and IFN-γ-expressing lymph node cells were dramatically decreased in curcumin-treated mice. In contrast, CD4+Foxp3+ splenocytes were increased in the curcumin-treated acute GVHD animals. Flow cytometric analysis revealed that animals transplanted with curcumin-treated allogeneic splenocytes showed increased populations of CD4+ regulatory T cells (Tregs) as well as CD8+ Treg cells, compared to animals administered vehicle-treated splenocytes. Curcumin-treated acute GVHD animals could have a change in B cell subpopulations. Conclusion/Significance In the present study, we investigated the efficacy and mechanism of action of curcumin treatment against acute GVHD. The acute GVHD mice administered with curcumin-treated splenocytes showed significantly reduced severity of acute GVHD. Curcumin exerted in vivo preventive effects on acute GVHD by reciprocal regulation of T helper 1 (Th1) and Treg (both CD4+ and CD8+ Treg) cell lineages as well as B cell homeostasis.
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