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  1. AU="Yeonsoo Joe"
  2. AU="Christina Drake"
  3. AU="Rosenbloom, E Scott"
  4. AU="Clémentine Schilte"
  5. AU="Montanari, Andrea"
  6. AU="Salehi Karizmeh, Mojtaba"
  7. AU="Svanberg Frisinger, Frida"
  8. AU="Iyappan, Petchi"
  9. AU="Naomi Nakagata"
  10. AU="Marianne A. van der Sande"
  11. AU="Reno, Chiara"

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  1. Artikel: Carbon monoxide induces the assembly of stress granule through the integrated stress response

    Chen, Yingqing / Yeonsoo Joe / Jeongmin Park / Hyun-Chul Song / Uh-Hyun Kim / Hun Taeg Chung

    Biochemical and biophysical research communications. 2019 Apr. 30, v. 512, no. 2

    2019  

    Abstract: Stress granules (SGs) are membraneless and phase-dense organelles that form transiently in response to a variety of harmful stimuli, including oxidative, heat, osmotic, ultraviolet light and chemotoxic stresses, and thus providing protective effects, ... ...

    Abstract Stress granules (SGs) are membraneless and phase-dense organelles that form transiently in response to a variety of harmful stimuli, including oxidative, heat, osmotic, ultraviolet light and chemotoxic stresses, and thus providing protective effects, allowing survivals. Carbon monoxide (CO), a gaseous second messenger, is synthesized by heme-oxygenases, and exerts anti-inflammatory, anti-proliferative and anti-apoptotic effects in a variety of cellular- and tissue-injury models. Several reports indicate that low levels of mitochondrial reactive oxygen species (mtROS) generated by CO can selectively activate PERK-eIF2α integrated stress response (ISR) to preserve the cellular homeostasis. Hence, CO can confer protection against cellular stresses. However, the mechanisms underlying the cyto-protective effects of CO against various harmful stimuli remain to be elucidated. Here, we sought to examine whether CO induces the SG assembly, and uncover its molecular mechanisms. We treated WI-38 cells and primary mouse embryonic fibroblasts (MEFs) with CO-releasing molecule 2 (CORM2) or CO gas, and found the SG assemblies were gradually increased in time and dose dependent manners. Next, we used Mito-TEMPO, an mtROS scavenger, to explore if mtROS might be involved in the CO-induced SG assembly. Furthermore, we confirmed the involvement of ISR consisted of PERK-eIF2α signaling pathway induced by CO for the SGs assembly. Finally, the inhibition of SG assembly by ISR inhibitor further verified CO-induced ISR might be responsible for SG. Taken together, in this study, we first demonstrated that CO is a novel SG inducer by activating ISR. Moreover, mtROS might be an initiator for the CO-induced ISR responsible for SG assembly.
    Schlagwörter apoptosis ; carbon monoxide ; cytoplasmic granules ; dose response ; fibroblasts ; heat ; heme oxygenase (biliverdin-producing) ; homeostasis ; mice ; mitochondria ; models ; protective effect ; reactive oxygen species ; signal transduction ; stress response ; ultraviolet radiation
    Sprache Englisch
    Erscheinungsverlauf 2019-0430
    Umfang p. 289-294.
    Erscheinungsort Elsevier Inc.
    Dokumenttyp Artikel
    ZDB-ID 205723-2
    ISSN 0006-291X ; 0006-291X
    ISSN (online) 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2019.03.017
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  2. Artikel: Impaired insulin signaling upon loss of ovarian function is associated with a reduction of tristetraprolin and an increased stabilization of chemokine in adipose tissue

    Choi, Eun-Kyung / Monisha Rajasekaran / Ok-Joo Sul / Yeonsoo Joe / Hyun-Taeg Chung / Rina Yu / Hye-Seon Choi

    Molecular and cellular endocrinology. 2018 Feb. 05, v. 461

    2018  

    Abstract: Loss of ovarian function can activate inflammation and lead to insulin resistance (IR). IR is also a core feature of obesity and obesity-associated metabolic dysfunction. Tristetraprolin/zinc finger protein 36 (TTP) interferes with TNF-α production by ... ...

    Abstract Loss of ovarian function can activate inflammation and lead to insulin resistance (IR). IR is also a core feature of obesity and obesity-associated metabolic dysfunction. Tristetraprolin/zinc finger protein 36 (TTP) interferes with TNF-α production by destabilizing TNF-α mRNA, and mice deficient in TTP develop a complex syndrome of inflammatory disease (Carballo et al., 1998; Taylor et al., 1999). We hypothesized that ovariectomy (OVX) might also prime inflammation by reducing tristetraprolin/zinc finger protein 36 (TTP) levels. We used a mouse OVX model to study impaired insulin signaling due to loss of ovarian function by evaluating Akt activity upon insulin stimulus. Impaired insulin signaling was initially detected in adipose tissue (AT) at 4 weeks after OVX, and then spread to liver and muscle, finally resulting in systemic IR at 12 weeks after OVX. OVX decreased TTP protein levels and increased adipocyte size, oxidative stress, chemokine expression and fat mass in AT by 4 weeks after surgery. TTP deficiency due to TTP gene deletion induced aberrant insulin signaling and increased chemokine expression and macrophage numbers in AT but did not increase adipocyte size, oxidative stress, or fat mass, suggesting that it promotes insulin signaling by decreasing AT inflammation independent of oxidative stress and adiposity. OVX, like TTP deficiency, increased the stability of chemokine transcripts as assessed from their half-lives. Our data indicate that the impaired insulin signaling resulting from OVX is due to an OVX-induced reduction of TTP and the resulting stabilization of inflammatory chemokines.
    Schlagwörter adipocytes ; adipose tissue ; adiposity ; chemokines ; gene deletion ; half life ; inflammation ; insulin ; liver ; macrophages ; messenger RNA ; mice ; models ; muscles ; obesity ; ovariectomy ; oxidative stress ; tumor necrosis factor-alpha ; zinc finger motif
    Sprache Englisch
    Erscheinungsverlauf 2018-0205
    Umfang p. 122-131.
    Erscheinungsort Elsevier B.V.
    Dokumenttyp Artikel
    ZDB-ID 187438-x
    ISSN 1872-8057 ; 0303-7207
    ISSN (online) 1872-8057
    ISSN 0303-7207
    DOI 10.1016/j.mce.2017.09.002
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  3. Artikel ; Online: Cross-talk between CD38 and TTP Is Essential for Resolution of Inflammation during Microbial Sepsis

    Yeonsoo Joe / Yingqing Chen / Jeongmin Park / Hyo Jeong Kim / So-Young Rah / Jinhyun Ryu / Gyeong Jae Cho / Hye-Seon Choi / Stefan W. Ryter / Jeong Woo Park / Uh-Hyun Kim / Hun Taeg Chung

    Cell Reports, Vol 30, Iss 4, Pp 1063-1076.e

    2020  Band 5

    Abstract: Summary: The resolution phase of acute inflammation is essential for tissue homeostasis, yet the underlying mechanisms remain unclear. We demonstrate that resolution of inflammation involves interactions between CD38 and tristetraprolin (TTP). During the ...

    Abstract Summary: The resolution phase of acute inflammation is essential for tissue homeostasis, yet the underlying mechanisms remain unclear. We demonstrate that resolution of inflammation involves interactions between CD38 and tristetraprolin (TTP). During the onset of acute inflammation, CD38 levels are increased, leading to the production of Ca2+-signaling messengers, nicotinic acid adenine dinucleotide phosphate (NAADP), ADP ribose (ADPR), and cyclic ADPR (cADPR) from NAD(P)+. To initiate the onset of resolution, TTP expression is increased by the second messengers, NAADP and cADPR, which downregulate CD38 expression. The activation of TTP by Sirt1-dependent deacetylation, in response to increased NAD+ levels, suppresses the acute inflammatory response and decreases Rheb expression, inhibits mTORC1, and induces autophagolysosomes for bacterial clearance. TTP may represent a mechanistic target of anti-inflammatory agents, such as carbon monoxide. TTP mediates crosstalk between acute inflammation and autophagic clearance of bacteria from damaged tissue in the resolution of inflammation during sepsis. : Sepsis as a clinical syndrome is characterized by systemic inflammation and widespread tissue injury. Joe et al. suggest that the activation of TTP, an RNA binding protein, helps to ameliorate the inflammatory response and promote bacterial clearance in sepsis. Keywords: acute inflammation, autophagolysosome, CD38, Rheb, resolution of inflammation, sepsis, Sirt1, tristetraprolin
    Schlagwörter Biology (General) ; QH301-705.5
    Sprache Englisch
    Erscheinungsdatum 2020-01-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: Induction of Heme Oxygenase-1 with Hemin Reduces Obesity-Induced Adipose Tissue Inflammation via Adipose Macrophage Phenotype Switching

    Thai Hien Tu / Yeonsoo Joe / Hye-Seon Choi / Hun Taeg Chung / Rina Yu

    Mediators of Inflammation, Vol

    2014  Band 2014

    Schlagwörter Pathology ; RB1-214 ; Medicine ; R
    Sprache Englisch
    Erscheinungsdatum 2014-01-01T00:00:00Z
    Verlag Hindawi Publishing Corporation
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  5. Artikel ; Online: Induction of Heme Oxygenase-1 with Hemin Reduces Obesity-Induced Adipose Tissue Inflammation via Adipose Macrophage Phenotype Switching

    Thai Hien Tu / Yeonsoo Joe / Hye-Seon Choi / Hun Taeg Chung / Rina Yu

    Mediators of Inflammation, Vol

    2014  Band 2014

    Schlagwörter Pathology ; RB1-214 ; Medicine ; R
    Sprache Englisch
    Erscheinungsdatum 2014-01-01T00:00:00Z
    Verlag Hindawi Publishing Corporation
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel ; Online: Induction of Heme Oxygenase-1 with Hemin Reduces Obesity-Induced Adipose Tissue Inflammation via Adipose Macrophage Phenotype Switching

    Thai Hien Tu / Yeonsoo Joe / Hye-Seon Choi / Hun Taeg Chung / Rina Yu

    Mediators of Inflammation, Vol

    2014  Band 2014

    Schlagwörter Pathology ; RB1-214 ; Medicine ; R
    Sprache Englisch
    Erscheinungsdatum 2014-01-01T00:00:00Z
    Verlag Hindawi Publishing Corporation
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  7. Artikel ; Online: Cilostazol attenuates ovariectomy-induced bone loss by inhibiting osteoclastogenesis.

    Ke Ke / Ali Muhammad Safder / Ok-Joo Sul / Jae-Hee Suh / Yeonsoo Joe / Hun-Taeg Chung / Hye-Seon Choi

    PLoS ONE, Vol 10, Iss 5, p e

    2015  Band 0124869

    Abstract: Cilostazol has been reported to alleviate the metabolic syndrome induced by increased intracellular adenosine 3',5'-cyclic monophosphate (cAMP) levels, which is also associated with osteoclast (OC) differentiation. We hypothesized that bone loss might be ...

    Abstract Cilostazol has been reported to alleviate the metabolic syndrome induced by increased intracellular adenosine 3',5'-cyclic monophosphate (cAMP) levels, which is also associated with osteoclast (OC) differentiation. We hypothesized that bone loss might be attenuated via an action on OC by cilostazol.To test this idea, we investigated the effect of cilostazol on ovariectomy (OVX)-induced bone loss in mice and on OC differentiation in vitro, using μCT and tartrate-resistant acid phosphatase staining, respectively. Cilostazol prevented from OVX-induced bone loss and decreased oxidative stress in vivo. It also decreased the number and activity of OC in vitro. The effect of cilostazol on reactive oxygen species (ROS) occurred via protein kinase A (PKA) and cAMP-regulated guanine nucleotide exchange factor 1, two major effectors of cAMP. Knockdown of NADPH oxidase using siRNA of p47phox attenuated the inhibitory effect of cilostazol on OC formation, suggesting that decreased OC formation by cilostazol was partly due to impaired ROS generation. Cilostazol enhanced phosphorylation of nuclear factor of activated T cells, cytoplasmic 1 (NFAT2) at PKA phosphorylation sites, preventing its nuclear translocation to result in reduced receptor activator of nuclear factor-κB ligand-induced NFAT2 expression and decreased binding of nuclear factor-κB-DNA, finally leading to reduced levels of two transcription factors required for OC differentiation.Our data highlight the therapeutic potential of cilostazol for attenuating bone loss and oxidative stress caused by loss of ovarian function.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2015-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  8. Artikel ; Online: The involvement of 4‐1BB/4‐1BBL signaling in glial cell‐mediated hypothalamic inflammation in obesity

    Jiye Kim / Yoon‐Hee Kwon / Chu‐Sook Kim / Thai H. Tu / Byung‐Sam Kim / Yeonsoo Joe / Hun T. Chung / Tsuyoshi Goto / Teruo Kawada / Taesun Park / Myung‐Sook Choi / Min‐Seon Kim / Rina Yu

    FEBS Open Bio, Vol 8, Iss 5, Pp 843-

    2018  Band 853

    Abstract: Obesity‐induced inflammation occurs not only in peripheral tissues but also in areas of the central nervous system. Glial cells such as astrocytes and microglia play crucial roles in obesity‐related hypothalamic inflammation, leading to the derangement ... ...

    Abstract Obesity‐induced inflammation occurs not only in peripheral tissues but also in areas of the central nervous system. Glial cells such as astrocytes and microglia play crucial roles in obesity‐related hypothalamic inflammation, leading to the derangement of energy metabolism and neurodegenerative pathologies. Here, we show that the interaction of 4‐1BB/4‐1BBL between lipid‐laden astrocytes/microglia promotes hypothalamic inflammation in obesity. Stimulation of 4‐1BB, a member of the TNF receptor superfamily, and/or its ligand 4‐1BBL on astrocytes and/or microglia with a specific agonist resulted in activation of the inflammatory signaling pathway and enhanced production of inflammatory mediators. Contact coculture of lipid‐laden astrocytes and microglia increased the production of inflammatory mediators, and blockade of the 4‐1BB/4‐1BBL interaction reduced the inflammatory response. Moreover, deficiency of 4‐1BB reduced hypothalamic inflammation in obese mice fed an high‐fat diet. These findings suggest that 4‐1BBL/4‐1BB signaling enhances the glial cell‐mediated inflammatory cross talk and participates in obesity‐induced hypothalamic inflammation.
    Schlagwörter hypothalamus ; inflammation ; obesity ; Biology (General) ; QH301-705.5
    Sprache Englisch
    Erscheinungsdatum 2018-05-01T00:00:00Z
    Verlag Wiley
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  9. Artikel: Hemeoxygenase-1 maintains bone mass via attenuating a redox imbalance in osteoclast

    Ke, Ke / Hun-Taeg Chung / Hye-Seon Choi / Jae-Hee Suh / M.A. Safder / Ok-Joo Sul / Woon-Ki Kim / Yeonsoo Joe

    Molecular and Cellular Endocrinology. 2015 July 05, v. 409

    2015  

    Abstract: Heme oxygenase-1 (HO-1) has long been considered to be an endogenous antioxidant. However, the role of HO-1 is highly controversial in developing metabolic diseases. We hypothesized that HO-1 plays a role in maintaining bone mass by alleviating a redox ... ...

    Abstract Heme oxygenase-1 (HO-1) has long been considered to be an endogenous antioxidant. However, the role of HO-1 is highly controversial in developing metabolic diseases. We hypothesized that HO-1 plays a role in maintaining bone mass by alleviating a redox imbalance. We investigated its role in bone remodeling. The absence of HO-1 in mice led to decreased bone mass with elevated activity and number of OCs, as well as higher serum levels of reactive oxygen species (ROS). HO-1, which is constitutively expressed at a high level in osteoclast (OC) precursors, was down-regulated during OC differentiation. HO-1 deficiency in bone marrow macrophages (BMM) in vitro resulted in increased numbers and activity of OCs due to enhanced receptor activator of nuclear factor-κB ligand (RANKL) signaling. This was associated with increased activation of nuclear factor-κB and of nuclear factor of activated T-cells, cytoplasmic 1 along with elevated levels of intracellular calcium and ROS. Decreased bone mass in the absence of HO-1 appears to be mainly due to increased osteoclastogenesis and bone resorption resulting from elevated RANKL signaling in OCs. Our data highlight the potential role of HO-1 in maintaining bone mass by negatively regulating OCs.
    Schlagwörter antioxidants ; blood serum ; bone density ; bone marrow ; bone resorption ; calcium ; gene expression ; heme oxygenase (biliverdin-producing) ; ligands ; macrophages ; metabolic diseases ; mice ; osteoclasts ; reactive oxygen species ; T-lymphocytes ; transcription factor NF-kappa B
    Sprache Englisch
    Erscheinungsverlauf 2015-0705
    Umfang p. 11-20.
    Erscheinungsort Elsevier Ireland Ltd
    Dokumenttyp Artikel
    ZDB-ID 187438-x
    ISSN 1872-8057 ; 0303-7207
    ISSN (online) 1872-8057
    ISSN 0303-7207
    DOI 10.1016/j.mce.2015.03.022
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  10. Artikel ; Online: Inhibitory Effects of Chung Hun Wha Dam Tang (CHWDT) on High-Fat Diet-Induced Obesity via AMP-Activated Protein Kinase Activation

    Md. Jamal Uddin / Yeonsoo Joe / Min Zheng / Sena Kim / Hoyoung Lee / Tae-Oh Kwon / Hun Taeg Chung

    Evidence-Based Complementary and Alternative Medicine, Vol

    2012  Band 2012

    Abstract: The Chung Hun Wha Dam Tang (CHWDT) herbal combination was reported to cease dizziness and phlegm. However, the effect of CHWDT in obesity has not yet been known mechanically. Therefore, we investigated whether this CHWDT could protect the cells from ... ...

    Abstract The Chung Hun Wha Dam Tang (CHWDT) herbal combination was reported to cease dizziness and phlegm. However, the effect of CHWDT in obesity has not yet been known mechanically. Therefore, we investigated whether this CHWDT could protect the cells from lipogenesis, gluconeogenesis, and inflammation in both in vivo and in vitro. CHWDT significantly decreased body weight, epididymal and perirenal fat content without affecting feed intake in high-fat diet-induced obese mice model. Additionally, CHWDT inhibited obesity-induced SREBP1, FAS, PGC1α, G6Pase, PEPCK and increased CPT1, ACO, and LCAD genes expression in vivo and in vitro. Proinflammatory cytokines like TNF-α and iNOS expression were reduced by CHWDT in both Raw264.7 macrophages and HepG2 cells. In addition, NO production was also significantly decreased by CHWDT in LPS-stimulated macrophages. Furthermore, AMPKα activation by CHWDT was involved in inhibition of obesity by reducing triglycerides production and increasing CPT1 expression. Based on all of the results, we suggest that CHWDT has inhibitory effects on obesity-induced lipogenesis, gluconeogenesis, and inflammation via AMPKα activation.
    Schlagwörter Other systems of medicine ; RZ201-999
    Sprache Englisch
    Erscheinungsdatum 2012-01-01T00:00:00Z
    Verlag Hindawi Limited
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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