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Kim, Sena,Joe, Yeonsoo,Kim, Hyo Jeong,Kim, You-Sun,Jeong, Sun Oh,Pae, Hyun-Ock,Ryter, Stefan W.,Surh, Young-Joon,Chung, Hun Taeg The American Association of Immunologists, Inc. 2015 JOURNAL OF IMMUNOLOGY Vol.194 No.9
<P>IL-1 beta and TNF-alpha are important proinflammatory cytokines that respond to mutated self-antigens of tissue damage and exogenous pathogens. The endoplasmic reticulum (ER) stress and unfolded protein responses are related to the induction of proinflammatory cytokines. However, the detailed molecular pathways by which ER stress mediates cytokine gene expression have not been investigated. In this study, we found that ER stress-induced inositol-requiring enzyme (IRE) 1a activation differentially regulates proinflammatory cytokine gene expression via activation of glycogen synthase kinase (GSK)-3 beta and X-box binding protein (XBP)-1. Surprisingly, IL-1 beta gene expression was modulated by IRE1 alpha-mediated GSK-3 beta activation, but not by XBP-1. However, IRE1 alpha-mediated XBP-1 splicing regulated TNF-alpha gene expression. SB216763, a GSK-3 inhibitor, selectively inhibited IL-1 beta gene expression, whereas the IRE1 alpha RNase inhibitor STF083010 suppressed only TNF-alpha production. Additionally, inhibition of GSK-3 beta greatly increased IRE1 alpha-dependent XBP-1 splicing. Our results identify an unsuspected differential role of downstream mediators GSK-3 beta and XBP-1 in ER stress-induced IRE1 alpha activation that regulates cytokine production through signaling cross-talk. These results have important implications in the regulation of inflammatory pathways during ER stress, and they suggest novel therapeutic targets for diseases in which meta-inflammation plays a key role.</P>
FGF21 induced by carbon monoxide mediates metabolic homeostasis <i>via</i> the PERK/ATF4 pathway
Joe, Yeonsoo,Kim, Sena,Kim, Hyo Jeong,Park, Jeongmin,Chen, Yingqing,Park, Hyeok-Jun,Jekal, Seung-Joo,Ryter, Stefan W.,Kim, Uh Hyun,Chung, Hun Taeg Federation of American Societies for Experimental 2018 The FASEB Journal Vol. No.
<P>The prevalence of metabolic diseases, including type 2 diabetes, obesity, and cardiovascular disease, has rapidly increased, yet the molecular mechanisms underlying the metabolic syndrome, a primary risk factor, remain incompletely understood. The small, gaseous molecule carbon monoxide (CO) has well-known anti-inflammatory, antiproliferative, and antiapoptotic effects in a variety of cellular- and tissue-injury models, whereas its potential effects on the complex pathways of metabolic disease remain unknown. We demonstrate here that CO can alleviate metabolic dysfunction <I>in vivo</I> and <I>in vitro</I>. We show that CO increased the expression and section of the fibroblast growth factor 21 (FGF21) in hepatocytes and liver. CO-stimulated PERK activation and enhanced the levels of FGF21 <I>via</I> the eIF2α–ATF4 signaling pathway. The induction of FGF21 by CO attenuated endoreticulum stress- or diet-induced, obesity-dependent hepatic steatosis. Moreover, CO inhalation lowered blood glucose levels, enhanced insulin sensitivity, and promoted energy expenditure by stimulating the emergence of beige adipose cells from white adipose cells. In conclusion, we suggest that CO acts as a potent inducer of FGF21 expression and that CO critically depends on FGF21 to regulate metabolic homeostasis.—Joe, Y., Kim, S., Kim, H. J., Park, J., Chen, Y., Park, H.-J., Jekal, S.-J., Ryter, S. W., Kim, U. H., Chung, H. T. FGF21 induced by carbon monoxide mediates metabolic homeostasis <I>via</I> the PERK/ATF4 pathway.</P>
Rapid Identification of Jasmine Virus H Infecting Ixora coccinea by Nanopore Metatranscriptomics
Sung-Woong Kim(Sung-Woong Kim),Hyo-Jeong Lee(Hyo-Jeong Lee),Sena Choi(Sena Choi),In-Sook Cho(In-Sook Cho),Rae-Dong Jeong(Rae-Dong Jeong) 한국식물병리학회 2023 Plant Pathology Journal Vol.39 No.3
The global climate change and international trade have facilitated the movement of plants across borders, increasing the risk of introducing novel plant viruses in new territories. Ixora coccinea exhibited virus-like foliar symptoms, including mosaic and mild mottle. An Oxford Nanopore Technologies-based compact and portable MinION platform was used to identify the causal viral pathogen. The complete genome sequence of jasmine virus H (JaVH; 3867 nt, JaVH-CNU) was determined and found to share 88.4-90.3% nucleotide identity with that of Jasminum sambac JaVH isolate in China. Phylogenetic analysis based on the complete amino acid sequences of RNA-dependent RNA poly-merase and coat protein revealed that JaVH-CNU was grouped separately with other JaVH isolates. This is the first report of a natural JaVH infection of I. coccinea. The application of rapid nanopore sequencing for plant virus identification was demonstrated and is expected to provide accurate and rapid diagnosis for virus sur-veillance.
Do-Hyun Kim(Do-Hyun Kim),Rae-Dong Jeong(Rae-Dong Jeong),Sena Choi(Sena Choi),Ho-Jong Ju(Ho-Jong Ju),Ju-Yeon Yoon(Ju-Yeon Yoon) 한국식물병리학회 2022 Plant Pathology Journal Vol.38 No.6
Cymbidium mosaic virus (CymMV) is one of economically important viruses that cause significant losses of orchids in the world. In the present study, a reverse transcription recombinase polymerase amplification (RT-RPA) assay combined with a lateral flow immunostrip (LFI) assay was developed for the detection of CymMV in orchid plants. A pair of primers containing fluorescent probes at each terminus that amplifies highly specifically a part of the coat protein gene of CymMV was determined for RT-RPA assay. The RT-RPA assay involved incubation at an isothermal temperature (39°C) and could be performed rapidly within 30 min. In addition, no cross-reactivity was observed to occur with odontoglossum ringspot virus and cymbidium chlorotic mosaic virus. The RT-RPA with LFI assay (RT-RPA-LFI) for CymMV showed 100 times more sensitivity than conventional reverse transcription polymerase chain reaction (RT-PCR). Furthermore, the RT-PCR-LFI assay demonstrated the simplicity and the rapidity of CymMV detection since the assay did not require any equipment, by comparing results with those of conventional RT-PCR. On-site application of the RT-RPA-LFI assay was validated for the detection of CymMV in field-collected orchids, indicating a simple, rapid, sensitive, and reliable method for detecting CymMV in orchids.
Jeung Hee Lee,Chan Wook Son,Mi Yeon Kim,Min Hee Kim,Hye Ran Kim,Eun Shil Kwak,Sena Kim,Mee Ree Kim 한국영양학회 2009 Nutrition Research and Practice Vol.3 No.2
The effect of diet supplemented with red beet (Beta vulgaris L.) leaf on antioxidant status of plasma and tissue was investigated in C57BL/6J mice. The mice were randomly divided into two groups after one-week acclimation, and fed a high fat (20%) and high cholesterol (1%) diet without (control group) or with 8% freeze-dried red beet leaf (RBL group) for 4 weeks. In RBL mice, lipid peroxidation determined as 2-thiobarbituric acid-reactive substances (TBARS value) was significantly reduced in the plasma and selected organs (liver, heart, and kidney). Levels of antioxidants (glutathione and β-carotene) and the activities of antioxidant enzyme (glutathione peroxidase) in plasma and liver were considerably increased, suggesting that antioxidant defenses were improved by RBL diet. Comet parameters such as tail DNA (%), tail extent moment, olive tail moment and tail length were significantly reduced by 25.1%, 49.4%, 35.4%, and 23.7%, respectively, in plasma lymphocyte DNA of RBL mice compared with control mice, and indicated the increased resistance of lymphocyte DNA to oxidative damage. In addition, the RBL diet controlled body weight together with a significant reduction of fat pad (retroperitoneal, epididymal, inguinal fat, and total fat). Therefore, the present study suggested that the supplementation of 8% red beet leaf in high fat high cholesterol diet could prevent lipid peroxidation and improve antioxidant defense system in the plasma and tissue of C57BL/6J mice.
Kim, Doyun,Chung, Sena,Lee, Seung‐,Hyun,Choi, Se‐,Young,Kim, Soung‐,Min,Koo, JaeHyung,Lee, Jong‐,Ho,Jahng, Jeong Won CAROL DAVILA UNIVERSITY PRESS 2017 Journal of Cellular and Molecular Medicine Vol.21 No.12
<P><B>Abstract</B></P><P>The hypoglossal nerve controls tongue movements, and damages of it result in difficulty in mastication and food intake. Mastication has been reported to maintain hippocampus‐dependent cognitive function. This study was conducted to examine the effect of tongue motor loss on the hippocampus‐dependent cognitive function and its underlying mechanism. Male Sprague Dawley rats were subjected to the initial training of Morris water maze task before or after the bilateral transection of hypoglossal nerves (Hx). When the initial training was given before the surgery, the target quadrant dwelling time during the probe test performed at a week after the surgery was significantly reduced in Hx rats relative to sham‐operated controls. When the initial training was given after the surgery, Hx affected the initial and reversal trainings and probe tests. Brain‐derived neurotrophic factor (BDNF) expression, cell numbers and long‐term potentiation (LTP) were examined in the hippocampus on the 10<SUP>th</SUP> day, and BrdU and doublecortin staining on the 14<SUP>th</SUP> day, after the surgery. Hx decreased the hippocampal BDNF and cells in the CA1/CA3 regions and impaired LTP. BrdU and doublecortin staining was decreased in the dentate gyrus of Hx rats. Results suggest that tongue motor loss impairs hippocampus‐dependent cognitive function, and decreased BDNF expression in the hippocampus may be implicated in its underlying molecular mechanism in relation with decreased neurogenesis/proliferation and impaired LTP.</P>
Kim, Sena,Joe, Yeonsoo,Surh, Young-Joon,Chung, Hun Taeg Hindawi 2018 Oxidative medicine and cellular longevity Vol.2018 No.-
<P>The ability of the host immune response is largely mediated by the proinflammatory cytokine production. Physiological and pathological conditions of endoplasmic reticulum (ER) trigger unfolded protein response and contribute to the development or pathology of inflammatory diseases. Under ER stress, unfolded protein response (UPR) signaling pathways participate in upregulating inflammatory cytokine production via NF-kappaB, MAPK, and GSK-3<I>β</I>. Moreover, it has been suggested that ER stress crosstalks with toll-like receptor (TLR) signaling pathway to promote the production of proinflammatory cytokines. In addition, TLR stimulation can lead to UPR activation to promote inflammation. In this review, we will cover how proinflammatory cytokine production by UPR signaling can be induced or amplified in the presence or absence of TLR activation.</P>