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Hong, Gyong Hwa,Kwon, Hyouk-Soo,Moon, Keun-Ai,Park, So Young,Park, Sunjoo,Lee, Kyoung Young,Ha, Eun Hee,Kim, Tae-Bum,Moon, Hee-Bom,Lee, Heung Kyu,Cho, You Sook American Association of Immunologists 2016 Journal of Immunology Vol. No.
<P>Recruitment and activation of dendritic cells (DCs) in the lungs are critical for Th2 responses in asthma, and CCL20 secreted from bronchial epithelial cells (BECs) is known to influence the recruitment of DCs. Because asthma is a disease that is closely associated with oxidative stress, we hypothesized that clusterin, an oxidative stress regulatory molecule, may have a role in the development of allergic airway inflammation. The aim of this study was to examine whether clusterin regulates CCL20 production from the BECs and the subsequent DC recruitment in the lungs. To verify the idea, clusterin knockout (Clu(-/-)), clusterin heterogeneous (Clu(+/-)), and wild-type mice were exposed intranasally to house dust mite (HDM) extract to induce allergic airway inflammation. We found that the total number of immune cells in bronchoalveolar lavage fluid and the lung was increased in Clu(-/-) and Clu(+/-) mice. Of these immune cells, inflammatory DCs (CD11b(+)CD11c(+)) and Ly6C(high) monocyte populations in the lung were significantly increased, which was accompanied by increased levels of various chemokines, including CCL20 in bronchoalveolar lavage fluid, and increased oxidative stress markers in the lung. Moreover, HDM-stimulated human BECs with either up- or downregulated clusterin expression showed that CCL20 secretion was negatively associated with clusterin expression. Interestingly, clusterin also reduced the level of intracellular reactive oxygen species, which is related to induction of CCL20 expression after HDM stimulation. Thus, the antioxidant property of clusterin is suggested to regulate the expression of CCL20 in BECs and the subsequent recruitment of inflammatory DCs in the airway.</P>
IL-32γ attenuates airway fibrosis by modulating the integrin-FAK signaling pathway in fibroblasts
Hong, Gyong Hwa,Park, So-Young,Kwon, Hyouk-Soo,Bang, Bo-Ram,Lee, Jaechun,Kim, Sang-Yeob,Pack, Chan-Gi,Kim, Soohyun,Moon, Keun-Ai,Kim, Tae-Bum,Moon, Hee-Bom,Cho, You Sook BioMed Central 2018 Respiratory research Vol.19 No.-
<P><B>Background</B></P><P>Fibrosis in severe asthma often leads to irreversible organ dysfunction. However, the mechanism that regulates fibrosis remains poorly understood. Interleukin (IL)-32 plays a role in several chronic inflammatory diseases, including severe asthma. In this study, we investigated whether IL-32 is involved in fibrosis progression in the lungs.</P><P><B>Methods</B></P><P>Murine models of chronic airway inflammation induced by ovalbumin and <I>Aspergillus melleus</I> protease and bleomycin-induced pulmonary fibrosis were employed. We evaluated the degree of tissue fibrosis after treatment with recombinant IL-32γ (rIL-32γ). Expression of fibronectin and α-smooth muscle actin (α-SMA) was examined and the transforming growth factor (TGF)-β-related signaling pathways was evaluated in activated human lung fibroblasts (MRC-5 cells) treated with rIL-32γ.</P><P><B>Results</B></P><P>rIL-32γ significantly attenuated collagen deposition and α-SMA production in both mouse models. rIL-32γ inhibited the production of fibronectin and α-SMA in MRC-5 cells stimulated with TGF-β. Additionally, rIL-32γ suppressed activation of the integrin-FAK-paxillin signaling axis but had no effect on the Smad and non-Smad signaling pathways. rIL-32γ localized outside of MRC-5 cells and inhibited the interaction between integrins and the extracellular matrix without directly binding to intracellular FAK and paxillin.</P><P><B>Conclusions</B></P><P>These results demonstrate that IL-32γ has anti-fibrotic effects and is a novel target for preventing fibrosis.</P><P><B>Electronic supplementary material</B></P><P>The online version of this article (10.1186/s12931-018-0863-3) contains supplementary material, which is available to authorized users.</P>
Quantum Key Distribution among Three Parties
Gyong-Luck Khym,Hyung-Jin Yang,Chang-Ho Hong,Hwa-Yeon Lee,Ji In Kim,Woo-Young Jung 한국물리학회 2004 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.44 No.6
We proposed a quantum key distribution (QKD) among three parties using Greenberger-Horne- Zeilinger (GHZ) states. In this scheme, two parties perform local unitary operations while the other party performs sequential operations composed of a CNOT (controlled-not) operation, a Bell state measurement, and a one-particle polarization measurement in order to identify the local unitary operations of the first two parties.
윤선영,Gyong Hwa Hong,권혁수,Sunjoo Park,박소영,신보미,김태범,문희범,조유숙 생화학분자생물학회 2016 Experimental and molecular medicine Vol.48 No.-
Increased oxidative stress has an important role in asthmatic airway inflammation and remodeling. A potent methyl donor, S-adenosylmethionine (SAMe), is known to protect against tissue injury and fibrosis through modulation of oxidative stress. The aim of this study was to evaluate the effect of SAMe on airway inflammation and remodeling in a murine model of chronic asthma. A mouse model was generated by repeated intranasal challenge with ovalbumin and Aspergillus fungal protease twice a week for 8 weeks. SAMe was orally administered every 24 h for 8 weeks. We performed bronchoalveolar lavage (BAL) fluid analysis and histopathological examination. The levels of various cytokines and 4-hydroxy-2-nonenal (HNE) were measured in the lung tissue. Cultured macrophages and fibroblasts were employed to evaluate the underlying anti-inflammatory and antifibrotic mechanisms of SAMe. The magnitude of airway inflammation and fibrosis, as well as the total BAL cell counts, were significantly suppressed in the SAMe-treated groups. A reduction in T helper type 2 pro-inflammatory cytokines and HNE levels was observed in mouse lung tissue after SAMe administration. Macrophages cultured with SAMe also showed reduced cellular oxidative stress and pro-inflammatory cytokine production. Moreover, SAMe treatment attenuated transforming growth factor-β (TGF-β)-induced fibronectin expression in cultured fibroblasts. SAMe had a suppressive effect on airway inflammation and fibrosis in a mouse model of chronic asthma, at least partially through the attenuation of oxidative stress and TGF-β-induced fibronectin expression. The results of this study suggest a potential role for SAMe as a novel therapeutic agent in chronic asthma.
( Sunyoung Yoon ),( Gyong Hwa Hong ),( Sunjoo Park ),( Tae Bum Kim ),( Hyouk Soo Kwon ),( So Young Park ),( Bomi Shin ),( Hyo Jung Kim ),( So Young Park ),( Hee Bom Moon ),( You Sook Cho ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
Background: Increased oxidative stress play an important role in the development and perpetuation of the asthmatic airway infl ammation. A potent methyl donor, S-adeno-sylmethionine (SAMe) is known to have protective function in liver injury and fibrosis through modulation of oxidative stress. The aim of this study is to evaluate the effect of SAMe on airway infi ammation in a murine asthmatic model. Methods: Asthmatic mice were generated by intranasal (i.n.) administration of ovalbumin (OVA) with fungal protease twice a week for 8 weeks and were challenged with aerosolized OVA. The asthmatic mice were divided into 3 groups and orally treated with vehicle, low dose SAMe (30mg/kg/day per mice), and high dose SAMe (150mg/kg/ day per mice) for each group before each OVA challenge. Bronchoalvelolar lavage (BAL) fluid analysis and histopathologic examination were performed to evaluate airway in fiammation. Various cytokine were quantified in lung tissue. Oxidized glutathione (GSSG) and markers of lipid peroxidation in lung tissue were also measured. Results: Infl ammatory cells in BAL fiuid, tissue infl ammation and fibrosis were reduced in both treatment groups and especially effective in high dose group. The pro-infl ammatory cytokines such as IL-5 and IL-13 also decreased in treatment groups. The levels of GSSG and markers of lipid peroxidation were reduced in treatment groups. Conclusions: These results demonstrated the suppressive effect of SAMe on airway infiammation and fibrosis in mouse model of asthma and suggest its potential as new therapeutic agent in asthma treatment.
Li, Chengbin,Li, Zhenghua,Oh, Hwa Yong,Hong, Gyong Hee,Park, Jin Seo,Kim, Ji Man Elsevier 2018 CATALYSIS TODAY - Vol.307 No.-
<P><B>Abstract</B></P> <P>Highly ordered mesoporous Cu-Mn-Ce ternary metal oxide materials with various Cu/Mn molar ratios were successfully synthesized by using a nano-casting method from a mesoporous silica template with a cubic <I>Ia</I>3<I>d</I> mesostructure. The ternary metal oxide materials were characterized by X-ray diffraction (XRD), N<SUB>2</SUB>-sorption, electron microscopy, Raman spectroscopy, H<SUB>2</SUB>-temperature programmed reduction and CO-temperature programmed desorption. The XRD results indicated that the materials did not show any diffraction peaks corresponding to copper and manganese oxides, ensuring the formation of Cu<I> <SUB>x</SUB> </I>Mn<SUB>0.2-<I>x</I> </SUB>Ce<SUB>0.8</SUB>O<SUB>2</SUB> (<I>x</I> =0–0.2). The WGS activity of the ternary metal oxide catalysts increased as the molar ratios of Cu/Mn increased. Among the catalysts, the mesoporous Cu<SUB>0.18</SUB>Mn<SUB>0.02</SUB>Ce<SUB>0.8</SUB>O<SUB>2</SUB> catalyst exhibited the best catalytic activity in low temperature range with zero methane yield. Moreover, this catalyst showed excellent catalytic stability during the reaction. The observed enhancement in the WGS performances were attributed to high surface area, uniform crystalline framework with increased structural defect, highly dispersed copper and manganese within the ceria lattice or on the surface, and strong metal support interaction.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Ordered mesoporous Cu-Mn-Ce ternary metal oxide catalyst showed an excellent WGS reaction performances. </LI> <LI> Copper and manganese, incorporated within the CeO<SUB>2</SUB> lattice, enhanced the activity. </LI> <LI> Mesoporous ternary metal oxides exhibited good nanostructural and catalytic stabilities. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Progranulin protects lung epithelial cells from cigarette smoking‐induced apoptosis
Lee, Kyoung Young,Park, So‐,Young,Park, Sunjoo,Hong, Gyong Hwa,Moon, Keun‐,Ai,Kim, You‐,Sun,Oh, Yeon‐,Mok,Kwon, Hyouk‐,Soo,Kim, Tae‐,Bum,Moon, Hee‐,Bom,Cho, Y John Wiley Sons, Ltd 2017 RESPIROLOGY Vol.22 No.6
<P><B>ABSTRACT</B></P><P><B>Background and objective</B></P><P>Emphysema is characterized by irreversible destruction of alveolar walls with distal air space enlargement. Cigarette smoke (CS) is considered a major risk factor for emphysematous changes in COPD. Progranulin (PGRN), a glycoprotein induced by CS, has been reported to participate in apoptosis. However, the precise role of PGRN in emphysema is currently unknown. This study aimed to evaluate the role of PGRN in human alveolar epithelial cells (AECs) in response to CS.</P><P><B>Methods</B></P><P>First, PGRN expression was assessed in a mouse model of CS‐induced emphysema and in AECs after exposure to CS extract (CSE). Then, the effect of PGRN on CSE‐mediated apoptosis was determined under PGRN silencing or overexpressing conditions. To investigate the functional mechanism of PGRN, endoplasmic reticulum (ER) stress markers and the mitogen‐activated protein kinase (MAPK) pathway were also evaluated in the CSE‐exposed cells. Finally, PGRN expression levels in sera and peripheral blood mononuclear cells (PBMCs) were measured and compared between patients with COPD and healthy subjects.</P><P><B>Results</B></P><P>Our results revealed that PGRN expression was elevated in CS‐exposed mouse lungs and CSE‐treated AECs. CSE‐induced cellular apoptosis was significantly increased in PGRN‐knockdown AECs and decreased in PGRN‐overexpression cells. The activation of ER stress‐associated molecules correlated with PGRN expression levels. Compared with healthy controls, COPD patients exhibited significantly lower PGRN serum levels and higher PBMC intracellular PGRN levels.</P><P><B>Conclusion</B></P><P>PGRN in airway epithelial cells may regulate CS‐induced AEC apoptosis and may be involved in the development of COPD.</P>