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A Systems Approach for Decoding Mitochondrial Retrograde Signaling Pathways
Chae, Sehyun,Ahn, Byung Yong,Byun, Kyunghee,Cho, Young Min,Yu, Myeong-Hee,Lee, Bonghee,Hwang, Daehee,Park, Kyong Soo AAAS 2013 Science signaling Vol.6 No.264
<P><B>Signaling Mitochondrial Dysfunction</B></P><P>The mitochondrial and nuclear genomes contribute to mitochondrial function, and when mitochondrial function is compromised, mitochondrial retrograde signaling alters nuclear gene expression. Chae <I>et al</I>. performed gene expression profiling of engineered cells that had mitochondria containing a disease-associated mutation that causes mitochondrial dysfunction. By generating networks of transcription factors that targeted these genes, the authors revealed putative mitochondrial retrograde signaling pathways. One such pathway involved retinoic X receptor α (RXRA), the mRNA for which was reduced in the mutant cells. Network analysis and experiments in cells suggested that mitochondrial dysfunction caused by the mutation initiated a positive feedback loop that aggravated mitochondrial dysfunction: Reduced RXRA abundance further compromised expression of genes encoding products involved in mitochondrial function and translation. This gene transcription factor mapping network approach may reveal targets for therapeutic intervention of diseases associated with mitochondrial dysfunction.</P>
Multi-dimensional histone methylations for coordinated regulation of gene expression under hypoxia
Lee, Seongyeol,Lee, Jieon,Chae, Sehyun,Moon, Yunwon,Lee, Ho-Youl,Park, Bongju,Yang, Eun Gyeong,Hwang, Daehee,Park, Hyunsung Oxford University Press 2017 Nucleic acids research Vol.45 No.20
<P><B>Abstract</B></P><P>Hypoxia increases both active and repressive histone methylation levels via decreased activity of histone demethylases. However, how such increases coordinately regulate induction or repression of hypoxia-responsive genes is largely unknown. Here, we profiled active and repressive histone tri-methylations (H3K4me3, H3K9me3, and H3K27me3) and analyzed gene expression profiles in human adipocyte-derived stem cells under hypoxia. We identified differentially expressed genes (DEGs) and differentially methylated genes (DMGs) by hypoxia and clustered the DEGs and DMGs into four major groups. We found that each group of DEGs was predominantly associated with alterations in only one type among the three histone tri-methylations. Moreover, the four groups of DEGs were associated with different TFs and localization patterns of their predominant types of H3K4me3, H3K9me3 and H3K27me3. Our results suggest that the association of altered gene expression with prominent single-type histone tri-methylations characterized by different localization patterns and with different sets of TFs contributes to regulation of particular sets of genes, which can serve as a model for coordinated epigenetic regulation of gene expression under hypoxia.</P>
Kim, Su-Jin,Chae, Sehyun,Kim, Hokeun,Mun, Dong-Gi,Back, Seunghoon,Choi, Hye Yeon,Park, Kyong Soo,Hwang, Daehee,Choi, Sung Hee,Lee, Sang-Won The American Society for Biochemistry and Molecula 2014 Molecular and Cellular Proteomics Vol.13 No.3
<P>Adipose tissue is increasingly recognized as an endocrine organ playing important pathophysiological roles in metabolic abnormalities, such as obesity, cardiovascular disease, and type 2 diabetes mellitus (T2DM). In particular, visceral adipose tissue (VAT), as opposed to subcutaneous adipose tissue, is closely linked to the pathogenesis of insulin resistance and T2DM. Despite the importance of VAT, its molecular signatures related to the pathogenesis of T2DM have not been systematically explored. Here, we present comprehensive proteomic analysis of VATs in drug-naïve early T2DM patients and subjects with normal glucose tolerance. A total of 4,707 proteins were identified in LC-MS/MS experiments. Among them, 444 increased in abundance in T2DM and 328 decreased. They are involved in T2DM-related processes including inflammatory responses, peroxisome proliferator-activated receptor signaling, oxidative phosphorylation, fatty acid oxidation, and glucose metabolism. Of these proteins, we selected 11 VAT proteins that can represent alteration in early T2DM patients. Among them, up-regulation of FABP4, C1QA, S100A8, and SORBS1 and down-regulation of ACADL and PLIN4 were confirmed in VAT samples of independent early T2DM patients using Western blot. In summary, our profiling provided a comprehensive basis for understanding the link of a protein profile of VAT to early pathogenesis of T2DM.</P>
Koo, Bo Kyung,Chae, Sehyun,Kim, Kristine M.,Kang, Min Jueng,Kim, Eunhee G.,Kwak, Soo Heon,Jung, Hye Seung,Cho, Young Min,Choi, Sung Hee,Park, Young Joo,Shin, Choong Ho,Jang, Hak C.,Shin, Chan Soo,Hwan American Diabetes Association 2014 Diabetes Vol.63 No.9
<P>Autoantibodies can facilitate diagnostic and therapeutic means for type 1 diabetes (T1DM). We profiled autoantibodies from serum samples of 16 T1DM patients, 16 type 2 diabetic (T2DM) patients, and 27 healthy control subjects with normal glucose tolerance (NGT) by using protein microarrays containing 9,480 proteins. Two novel autoantibodies, anti-EEF1A1 and anti-UBE2L3, were selected from microarrays followed by immunofluorescence staining of pancreas. We then tested the validity of the candidates by ELISA in two independent test cohorts: <I>1</I>) 95 adults with T1DM, 49 with T2DM, 11 with latent autoimmune diabetes in adults (LADA), 20 with Graves disease, and 66 with NGT and <I>2</I>) 33 children with T1DM and 34 healthy children. Concentrations of these autoantibodies were significantly higher in T1DM patients than in NGT and T2DM subjects (<I>P</I> < 0.01), which was also confirmed in the test cohort of children (<I>P</I> < 0.05). Prevalence of anti-EEF1A1 and anti-UBE2L3 antibodies was 29.5% and 35.8% in T1DM, respectively. Of note, 40.9% of T1DM patients who lack anti-GAD antibodies (GADA) had anti-EEF1A1 and/or anti-UBE2L3 antibodies. These were also detected in patients with fulminant T1DM but not LADA. Our approach identified autoantibodies that can provide a new dimension of information indicative of T1DM independent of GADA and new insights into diagnosis and classification of T1DM.</P>
Lee, Seung Hyeun,Kim, Sung-Woo,Lee, Sehyun,Kim, EunSub,Kim, Duck-Joong,Park, Sohyun,Lee, Eun Joo,Lee, Sang Yeub,Lee, Ji Sung,Lim, Chae Seung,Kim, Won-Ki,In, Kwang Ho Elsevier 2014 Chest Vol.146 No.5
<P>NBS LabChip G2-3 is a novel, ultrafast, chip-type portable real-time polymerase chain reaction (PCR) system. We evaluated the clinical usefulness of this system in detecting pulmonary TB and assessed its diagnostic performance compared with a conventional tube-type PCR system.</P>
Particle size-dependent Marangoni vortex phenomenon in the evaporating droplet system
Changdeok Seo(서창덕),Daeho Jang(장대호),Jongjin Chae(채종진),Sehyun Shin(신세현) 대한기계학회 2015 대한기계학회 춘추학술대회 Vol.2015 No.11
Dissolving surfactant in water causes a vortex flow near droplet edge and leads to uniform patterns of colloidal particle deposition after evaporation. Radially-outward capillary flow and radially-inward Marangoni flow drive this vortex flow. Recently, Still, T. et al discovered that the motions of particles are affected by initial concentrations of surfactant (Sodium dodecyl sulfate). In this paper, we observed that particle behaviors are also affected by the particle size. 3 different sizes of PS (polystyrene) particle samples had different behavior in a fixed initial concentration of surfactant (SDS) solution. 3㎛ particles rotated slowly and 1μm particles rotated quickly. However 5㎛ particles were not rotating. Therefore, we suggest that not only the initial concentration but also the suspended particle size should be considered an important factor of the vortex flow phenomenon. In addition, the behaviors of particles in an evaporating droplet system could be controlled by adjusting the initial concentration of surfactant and the particle size.
Yoo Seungbo,Jeong Yun Hee,Choi Hong-Hee,Chae Sehyun,Hwang Daehee,Shin Sung Jae,Ha Sang-Jun 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Chronic viral infection impairs systemic immunity in the host; however, the mechanism underlying the dysfunction of immune cells in chronic viral infection is incompletely understood. In this study, we studied the lineage differentiation of hematopoietic stem cells (HSCs) during chronic viral infection to elucidate the changes in dendritic cell (DC) differentiation and subsequent impact on T cell functionality using a chronic lymphocytic choriomeningitis virus (LCMV) infection model. We first investigated the lineage differentiation of HSCs in the bone marrow (BM) to elucidate the modulation of immune cell differentiation and found that the populations highly restrained in their differentiation were common myeloid progenitors (CMPs) and common dendritic cell progenitors (CDPs). Of interest, the main immune cells infected with LCMV Clone 13 (CL13) in the BM were CD11b/c+ myeloid DCs. We next characterized CD11b+ DCs that differentiated during chronic LCMV infection. These DCs displayed a less immunogenic phenotype than DCs in naive or acutely infected mice, showing low expression of CD80 but high expression of PD-L1, B7-H4, IDO, TGF-β, and IL-10. Consequently, these CD11b+ DCs induced less effective CD8+ T cells and more Foxp3+ regulatory T (Treg) cells. Furthermore, CD11b+ DCs generated during CL13 infection could not induce effective CD8+ T cells specific to the antigens of newly invading pathogens. Our findings demonstrate that DCs generated from the BM during chronic viral infection cannot activate fully functional effector CD8+ T cells specific to newly incoming antigens as well as persistent antigens themselves, suggesting a potential cause of the functional alterations in the T cell immune response during chronic viral infection.