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Search Results: 1 - 10 of 61738 matches for " Chul-Woo Yang "
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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.
Degradation of HER2/neu by ANT2 shRNA suppresses migration and invasiveness of breast cancer cells
Ji-Young Jang, Yoon-Kyung Jeon, Chul-Woo Kim
BMC Cancer , 2010, DOI: 10.1186/1471-2407-10-391
Abstract: We utilized an ANT2 vector-based RNA interference approach to inhibition of ANT2 expression, and the HER2/neu-overexpressing human breast cancer cell line, SK-BR3, was used throughout the study.In this study, ANT2 shRNA decreased HER2/neu protein levels by promoting degradation of HER2/neu protein through dissociation from heat shock protein 90 (HSP90). As a result, ANT2 shRNA induced inhibitory effects on the PI3K/Akt signaling pathway. Inhibition of PI3K/Akt signaling by ANT2 shRNA caused down-regulation of membrane-type 1 matrix metalloproteinase (MT1-MMP) and vascular endothelial growth factor (VEGF) expression, decreased matrix metalloproteinase 2 (MMP2) and MMP9 activity, and suppressed migration and invasion of breast cancer cells.These results indicate that knock-down of ANT2 by shRNA down-regulates HER2/neu through suppression of HSP90's function and inhibits the PI3K/Akt signaling pathway, resulting ultimately in suppressed migration and invasion of breast cancer cells.Breast cancer is the most common cancer among women in the western world and the second leading cause of cancer related death in women [1]. Gene amplification and/or overexpression of some oncogenes have been implicated in development and progression of breast cancers. HER2/neu (also known as ErbB2) is one of the best characterized oncogenes linked with poor prognosis of breast cancer [2]. Overexpression of HER2/neu is found in about 30% of human breast cancers and correlates with more aggressive tumors and greater resistance to cancer chemotherapy [3].The HER2/neu oncoprotein is a transmembrane receptor, belonging to the epidermal growth factor receptor family, with tyrosine kinase activity, resulting in intracellular signaling and activation of genes involved in cell growth, which is associated with shortened survival, enhanced aggressiveness, and other poor prognostic factors in breast cancer [4]. Activation of HER2/neu may trigger activation of downstream signaling pathways, such as the
Suppression of adenine nucleotide translocase-2 by vector-based siRNA in human breast cancer cells induces apoptosis and inhibits tumor growth in vitro and in vivo
Ji-Young Jang, Yun Choi, Yoon-Kyung Jeon, Chul-Woo Kim
Breast Cancer Research , 2008, DOI: 10.1186/bcr1857
Abstract: We utilized an ANT2-specific RNA interference approach to inhibit ANT2 expression for evaluating its antitumor effect in vitro and in vivo. Specifically, to investigate the therapeutic potential of ANT2 repression, we used a DNA vector-based RNA interference approach by expressing shRNA to knockdown ANT2 in breast cancer cell lines overexpressing ANT2.ANT2 shRNA treatment in breast cancer cell line MDA-MB-231 repressed cell growth as well as proliferation. In addition, cell cycle arrest, ATP depletion and apoptotic cell death characterized by the potential disruption of mitochondrial membrane were observed from the ANT2 shRNA-treated breast cancer cells. Apoptotic breast cancer cells transfected with ANT2 shRNA also induced a cytotoxic bystander effect that generates necrotic cell death to the neighboring cells. The intracellular levels of TNFα and TNF-receptor I were increased in ANT2 shRNA transfected cells and the bystander effect was partly blocked by anti-TNFα antibody. Ultimately, ANT2 shRNA effectively inhibited tumor growth in vivo.These results suggest that vector-based ANT2 RNA interference could be an efficient molecular therapeutic method for breast cancer with high expression of ANT2.Apoptosis can occur via a death receptor-mediated pathway or a mitochondrial pathway, and mitochondria-mediated apoptosis is initiated by multiple stimuli such as TNF, CD95 and stresses [1]. After receiving apoptotic signals, mitochondrial membrane permeability increases and the mediators such as cytochrome c and apoptosis-inducing factors are released to the cytoplasm, rapidly followed by the activations of caspase 9 and executive caspase 3 [2]. In healthy cells, mitochondrial membrane permeability is tightly controlled by voltage-dependent anion channels that are regulated by the interactions between Bcl2 family proteins [3,4].Adenine nucleotide translocase (ANT) is a nuclear-encoded protein abundantly located in the inner mitochondrial membrane, and the role of this prot
Over-expression of Adenine Nucleotide Translocase 1 (ANT1) Induces Apoptosis and Tumor Regression in vivo
Ji-Young Jang, Yun Choi, Yoon-Kyung Jeon, Khin Aung, Chul-Woo Kim
BMC Cancer , 2008, DOI: 10.1186/1471-2407-8-160
Abstract: We applied an ANT1 gene transfer approach to induce apoptosis and to evaluate the anti-tumor effect of ANT1 in a nude mouse model.We demonstrated that ANT1 transfection induced apoptosis of MDA-MB-231 cells, inactivated NF-κB activity, and increased Bax expression. ANT1-inducing apoptosis was accompanied by the disruption of mitochondrial membrane potential, cytochrome c release and the activation of caspases-9 and -3. Moreover, ANT1 transfection significantly suppressed tumor growth in vivo.Our results suggest that ANT1 transfection may be a useful therapeutic modality for the treatment of cancer.Apoptosis is a programmed form of cell death, and as such, differs fundamentally from cellular necrosis. Apoptosis is characterized by genetically-controlled cellular auto-digestion via the activation of endogenous proteases [1]. Apoptosis results in cytoskeletal disruption, cell shrinkage, membrane blebbing, nuclear condensation, and inter-nucleosomal DNA fragmentation [1,2]. Moreover, apoptosis is essentially required for the homeostasis of normal tissues and to manage cellular disruption caused by mutations. Hence, the disruption of the apoptotic process is involved in the pathogenesis of many human diseases, including viral infections, autoimmune diseases, and cancers. In particular, progressive perturbations of the normal apoptotic pathway occur during neoplastic transformation, progression, and metastasis [3], and thus apoptosis-related genes are attractive cancer treatment developmental targets [4].Adenine nucleotide translocase (ANT) participates in ATP-for-ADP exchange through the inner mitochondrial membrane, which supplies the cytoplasm with newly synthesized ATP for oxidative phosphorylation [5]. Recently, it has been reported that death receptor-initiated pathway, mediated by RIP, disrupts the interaction between cyclophilin D and ANT and permits the binding of zVAD.fmk (zVAD) to ANT, which prevents ANT from adopting the conformational c-state and subsequently
Short-hairpin RNA-induced suppression of adenine nucleotide translocase-2 in breast cancer cells restores their susceptibility to TRAIL-induced apoptosis by activating JNK and modulating TRAIL receptor expression
Ji-Young Jang, Yoon-Kyung Jeon, Yun Choi, Chul-Woo Kim
Molecular Cancer , 2010, DOI: 10.1186/1476-4598-9-262
Abstract: ANT2 shRNA treatment sensitized MCF7, T47 D, and BT474 cells to TRAIL-induced apoptosis by up-regulating the expression of TRAIL death receptors 4 and 5 (DR4 and DR5) and down-regulating the TRAIL decoy receptor 2 (DcR2). In MCF7 cells, ANT2 knockdown activated the stress kinase c-Jun N-terminal kinase (JNK), subsequently stabilizing and increasing the transcriptional activity of p53 by phosphorylating it at Thr81; it also enhanced the expression and activity of DNA methyltransferase 1 (DNMT1). ANT2 shRNA-induced overexpression of DR4/DR5 and TRAIL sensitization were blocked by a p53 inhibitor, suggesting that p53 activation plays an important role in the transcriptional up-regulation of DR4/DR5. However, ANT2 knockdown also up-regulated DR4/DR5 in the p53-mutant cell lines BT474 and T47 D. In MCF7 cells, ANT2 shRNA treatment led to DcR2 promoter methylation and concomitant down-regulation of DcR2 expression, consistent with the observed activation of DNMT1. Treatment of the cells with a demethylating agent or JNK inhibitor prevented the ANT2 shRNA-induced down-regulation of DcR2 and activation of both p53 and DNMT1. In in vivo experiments using nude mice, ANT2 shRNA caused TRAIL-resistant MCF7 xenografts to undergo TRAIL-induced cell death, up-regulated DR4/DR5, and down-regulated DcR2. Co-treatment with ANT2 shRNA and TRAIL efficiently suppressed tumor growth in these mice.ANT2 suppression by shRNA might be exploited to overcome TRAIL-resistance in cancer.Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL; also known as apo2 ligand) is a member of the TNF subfamily. TRAIL induces apoptosis by recognizing and binding to its cognate receptors on cell surfaces. These receptors are known as death receptor 4 (DR4; TRAIL receptor 1; TRAILR1) and death receptor 5 (DR5; TRAIL receptor 2; TRAILR2). Binding initiates conformational changes in the receptors and recruits an adaptor molecule (Fas-associated death domain) and initiator caspases (caspase-8 and
The C-terminal region of Bfl-1 sensitizes non-small cell lung cancer to gemcitabine-induced apoptosis by suppressing NF-κB activity and down-regulating Bfl-1
Min-Kyoung Kim, Yoon-Kyung Jeon, Jong-Kyu Woo, Yun Choi, Dae-Han Choi, Yeul-Hong Kim, Chul-Woo Kim
Molecular Cancer , 2011, DOI: 10.1186/1476-4598-10-98
Abstract: Lung cancer remains a leading cause of cancer-related death [1] despite the introduction of several types of cytotoxic agents. In non-small cell lung cancer (NSCLC), chemotherapy often achieves limited clinical improvements due to acquired drug resistance and intolerable toxicities. Gemcitabine (difluorodeoxycytidine hydrochloride, dFdC) is a deoxycytidine analogue that is converted in vivo into the active metabolites, difluorodeoxycytidine di- and triphosphate (dFdCDP, dFdCTP). DFdCDP acts by inhibiting ribonucleotide reductase, whereas dFdCTP is incorporated into DNA and prevents DNA synthesis, thereby inducing apoptosis. Gemcitabine has been approved by the Food and Drug Administration (FDA) as a treatment for advanced and metastatic pancreatic cancer, ovarian cancer, breast cancer, and NSCLC, alone or in combination with other drugs http://www.cancer.gov/cancertopics/druginfo/gemcitabinehydrochloride webcite. Clinical trials have demonstrated that gemcitabine prolongs survival and improves the quality of life of advanced NSCLC patients [2]. In fact, gemcitabine is considered to be one of the most effective agents for treating NSCLC. Previous studies have concluded that when used as a single agent, gemcitabine consistently yields response rates exceeding 20%. Furthermore, preclinical data indicate that when used with platinum compounds, such as, cisplatin or carboplatin, gemcitabine has synergistic anti-tumor effects [3,4].However, gemcitabine often fails to achieve adequate disease control due to intrinsic or acquired resistance of tumor cells. The following are representative examples of putative resistance mechanisms; NF-κB and PI3K/Akt pathway activation in pancreatic and breast cancer [5,6] the up-regulation of anti-apoptotic Bcl-2 protein in pancreatic cancer [7,8] the deficiency of human equilibrate nucleoside transporter 1 in NSCLC [9]and alterations of gemcitabine metabolizing enzymes [10-13]. Many of these chemo-resistant mechanisms involve interrupting
Different Patterns of Evolution in the Centromeric and Telomeric Regions of Group A and B Haplotypes of the Human Killer Cell Ig-Like Receptor Locus
Chul-Woo Pyo,Lisbeth A. Guethlein,Quyen Vu,Ruihan Wang,Laurent Abi-Rached,Paul J. Norman,Steven G. E. Marsh,Jeffrey S. Miller,Peter Parham,Daniel E. Geraghty
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0015115
Abstract: The fast evolving human KIR gene family encodes variable lymphocyte receptors specific for polymorphic HLA class I determinants. Nucleotide sequences for 24 representative human KIR haplotypes were determined. With three previously defined haplotypes, this gave a set of 12 group A and 15 group B haplotypes for assessment of KIR variation. The seven gene-content haplotypes are all combinations of four centromeric and two telomeric motifs. 2DL5, 2DS5 and 2DS3 can be present in centromeric and telomeric locations. With one exception, haplotypes having identical gene content differed in their combinations of KIR alleles. Sequence diversity varied between haplotype groups and between centromeric and telomeric halves of the KIR locus. The most variable A haplotype genes are in the telomeric half, whereas the most variable genes characterizing B haplotypes are in the centromeric half. Of the highly polymorphic genes, only the 3DL3 framework gene exhibits a similar diversity when carried by A and B haplotypes. Phylogenetic analysis and divergence time estimates, point to the centromeric gene-content motifs that distinguish A and B haplotypes having emerged ~6 million years ago, contemporaneously with the separation of human and chimpanzee ancestors. In contrast, the telomeric motifs that distinguish A and B haplotypes emerged more recently, ~1.7 million years ago, before the emergence of Homo sapiens. Thus the centromeric and telomeric motifs that typify A and B haplotypes have likely been present throughout human evolution. The results suggest the common ancestor of A and B haplotypes combined a B-like centromeric region with an A-like telomeric region.
Exosomes Derived from Mesenchymal Stem Cells Suppress Angiogenesis by Down-Regulating VEGF Expression in Breast Cancer Cells
Jong-Kuen Lee, Sae-Ra Park, Bong-Kwang Jung, Yoon-Kyung Jeon, Yeong-Shin Lee, Min-Kyoung Kim, Yong-Goo Kim, Ji-Young Jang, Chul-Woo Kim
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0084256
Abstract: Exosomes are small membrane vesicles released by a variety of cell types. Exosomes contain genetic materials, such as mRNAs and microRNAs (miRNAs), implying that they may play a pivotal role in cell-to-cell communication. Mesenchymal stem cells (MSCs), which potentially differentiate into multiple cell types, can migrate to the tumor sites and have been reported to exert complex effects on tumor progression. To elucidate the role of MSCs within the tumor microenvironment, previous studies have suggested various mechanisms such as immune modulation and secreted factors of MSCs. However, the paracrine effects of MSC-derived exosomes on the tumor microenvironment remain to be explored. The hypothesis of this study was that MSC-derived exosomes might reprogram tumor behavior by transferring their molecular contents. To test this hypothesis, exosomes from MSCs were isolated and characterized. MSC-derived exosomes exhibited different protein and RNA profiles compared with their donor cells and these vesicles could be internalized by breast cancer cells. The results demonstrated that MSC-derived exosomes significantly down-regulated the expression of vascular endothelial growth factor (VEGF) in tumor cells, which lead to inhibition of angiogenesis in vitro and in vivo. Additionally, miR-16, a miRNA known to target VEGF, was enriched in MSC-derived exosomes and it was partially responsible for the anti-angiogenic effect of MSC-derived exosomes. The collective results suggest that MSC-derived exosomes may serve as a significant mediator of cell-to-cell communication within the tumor microenvironment and suppress angiogenesis by transferring anti-angiogenic molecules.
Brain activation patterns associated with sexual orientation in homosexual male and female: a case study with 3.0T fMRI  [PDF]
Gwang-Won Kim, Gwang-Woo Jeong, Jong-Chul Yang
Journal of Biomedical Science and Engineering (JBiSE) , 2011, DOI: 10.4236/jbise.2011.43027
Abstract: This study was performed to clarify the sexual orien-tation in a 19-year-old homosexual male and a 20-year-old homosexual female by using a functional magnetic resonance imaging (fMRI) with viewing male and female erotic nude pictures. The sex hor-mone levels of the homosexual male and female were in the normal range of healthy heterosexual males and females, respectively. In both homosexuals more significant brain activities were observed while view-ing the nude pictures of the same genetic sex than those of the opposite sex in the frontal cortex, parietal cortex, occipital cortex, anterior cingulate gyrus, amygdala, midbrain, hippocampus, orbitofrontal cortex, parahippocampal gyrus, thalamus, globus pallidus, and putamen, which are known to be re-sponsive to sexual arousal. The homosexual male and female showed a tendency toward higher sexual arousal to the same genetic sex as comparison with the opposite sex. This finding may be useful to un-derstand the different neural mechanisms on sexual arousal in homosexuals.
Human Adipose Tissue Derived Mesenchymal Stem Cells Aggravate Chronic Cyclosporin Nephrotoxicity by the Induction of Oxidative Stress
Byung Ha Chung, Sun Woo Lim, Kyoung Chan Doh, Shang Guo Piao, Seong Beom Heo, Chul Woo Yang
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0059693
Abstract: The aim of this study was to investigate whether hATMSCs protect against cyclosporine (CsA)-induced renal injury. CsA (7.5 mg/kg) and hATMSCs (3×106/5 mL) were administered alone and together to rats for 4 weeks. The effect of hATMSCs on CsA-induced renal injury was evaluated by assessing renal function, interstitial fibrosis, infiltration of inflammatory cells, and apoptotic cell death. Four weeks of CsA-treatment produced typical chronic CsA-nephropathy. Combined treatment with CsA and hATMSCs did not prevent these effects and showed a trend toward further renal deterioration. To evaluate why hATMSCs aggravated CsA-induced renal injury, we measured oxidative stress, a major mechanism of CsA-induced renal injury. Both urine and serum 8-hydroxydeoxyguanosine(8-OHdG) levels were higher in the CsA+hATMSCs group than in the CsA group (P<0.05). An in vitro study showed similar results. Although the rate of apoptosis did not differ significantly between HK-2 cells cultured in hATMSCs-conditioned medium and those cultured in DMEM, addition of CsA resulted in greater apoptosis in HK-2 cells cultured in hATMSCs-conditioned medium. Addition of CsA increased oxidative stress in the hATMSCs-conditioned medium. The results of our study suggest that treatment with hATMSCs may aggravate CsA-induced renal injury because hATMSCs cause oxidative stress in the presence of CsA.
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