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Kim, Seung Hyeon,Zhong, Xiancai,Kim, Wonki,Kim, Kyeojin,Suh, Young‐,Ger,Kim, Chaekyun,Joe, Yeonsoo,Chung, Hun Taeg,Cha, Young‐,Nam,Surh, Young‐,Joon Federation of American Society for Experimental Bi 2018 The FASEB Journal Vol.32 No.4
<P>Resolution of inflammation that occurs after microbial infection or tissue damage is an important physiologic process in maintaining or restoring host homeostasis. Taurine chloramine (TauCl) is formed by a reaction between taurine and hypochlorite in leukocytes, and it is especially abundant in activated neutrophils that encounter an oxidative burst. As neutrophils undergo apoptosis, TauCl is released to the extracellular matrix at the inflamed sites, thereby affecting coexisting macrophages in the inflammatory microenvironment. In this study, we investigated the role of TauCl in phagocytosis by macrophages during resolution of fungal infection-induced inflammation. We found that exogenous TauCl substantially increased the phagocytic efficiency of macrophages through up-regulation of dectin-1, a receptor for fungal beta-1,3-glucans, which is present on the membrane of macrophages. Our previous studies demonstrated the induction of heme oxygenase-1 (HO-1) expression in murine peritoneal macrophages treated with TauCl. In the present study, knocking out HO-1 or pharmacologic inhibition of HO-1 with zinc protoporphyrin IX attenuated the TauCl-induced expression of dectin-1 and subsequent phagocytosis. Furthermore, carbon monoxide (CO), a by-product of the HO-1-catalyzed reaction, induced expression of dectin-1 and potentiated phagocytic capability of the macrophages, which appeared to be mediated through up-regulation of peroxisome proliferator-activated receptor . Taken together, induction of HO-1 expression and subsequent CO production by TauCl are essential for phagocytosis of fungi by macrophages. Our results suggest that TauCl has important roles in host defense against fungal infection and has therapeutic potential in the management of inflammatory diseases.</P>
Diastereoselective Total Synthesis of (−)-Galiellalactone
Kim, Taewoo,Han, Young Taek,An, Hongchan,Kim, Kyeojin,Lee, Jeeyeon,Suh, Young-Ger American Chemical Society 2015 Journal of organic chemistry Vol.80 No.24
<P>An enantioselective total synthesis of (-)-galiellalactone has been accomplished. The key features of the synthesis involve the highly stereoselective construction of the cis-trisubstituted cyclopentane intermediate by a Pd(0)-catalyzed cyclization, the stereospecific introduction of an angular hydroxyl group by Riley oxidation, and the efficient construction of the tricyclic system of (-)-galiellalactone via a combination of diastereoselective Hosomi-Sakurai crotylation and ring-closing metathesis (RCM)</P>
Total synthesis of (−)-deguelin <i>via</i> an iterative pyran-ring formation strategy
Lee, Seungbeom,An, Hongchan,Chang, Dong-Jo,Jang, Jaebong,Kim, Kyeojin,Sim, Jaehoon,Lee, Jeeyeon,Suh, Young-Ger The Royal Society of Chemistry 2015 Chemical communications Vol.51 No.43
<P>Enantioselective synthesis of (-)-deguelin was accomplished via an iterative pyran-ring formation approach. The key features involve the anionic addition of a chromene unit to aryloxy alkyl aldehyde for the double cyclization precursor and iterative pyran ring formation by Pd-catalyzed O-arylation and C-arylation, respectively.</P>
Sujin Lee,서영거,Sony Marharjan,Jong-Wha Jung,김남중,Kyeojin Kim,한영택,임창진,Hyun-Jung Choi,권영근 대한약학회 2012 Archives of Pharmacal Research Vol.35 No.3
Design, synthesis and insight into the structure-activity relationships (SAR) of phytosterol analogues as novel antiapoptotic agents are described. In particular, the non-branched alkyl chain at C24 and the pseudosugar moiety at C3 hydroxyl group turned out crucial for the inhibition of human umbilical vein endothelial cells (HUVEC) apoptosis.
Sac-0601 prevents retinal vascular leakage in a mouse model of diabetic retinopathy
Maharjan, Sony,Lee, Sujin,Agrawal, Vijayendra,Choi, Hyun-Jung,Maeng, Yong-Sun,Kim, Kyeojin,Kim, Nam-Jung,Suh, Young-Ger,Kwon, Young-Guen Elsevier 2011 european journal of pharmacology Vol.657 No.1
<P><B>Abstract</B></P><P>Endothelium integrity is important for the normal functioning of vessels, the disruption of which can lead to disease. The blood-retinal barrier required for normal retinal function is compromised in diabetic retinopathy, causing retinal vascular leakage. Previously, we demonstrated the ability of Sac-0601[((2R,3S)-3-acetoxy-6-((3S,10R,13R,17R)-10,13-dimethyl-17-((R)-6-methylheptan-2-yl)-2,3,4,7,8,9,10,11,12,13,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-3-yloxy)-3,6-dihydro-2H-pyran-2-yl)methyl acetate], a pseudo-sugar derivative of cholesterol, to increase survival of retinal endothelial cells. In the present study, we evaluated the ability of Sac-0601 to prevent retinal vascular leakages <I>in vitro</I> and <I>in vivo</I>. Sac-0601 treatment blocked VEGF-induced formation of actin stress fibers and stabilized the cortical actin ring in retinal endothelial cells. It also inhibited degradation of occludin, an important tight junction protein, and blocked VEGF-induced disruption of its linear pattern at the cell border. The [<SUP>14</SUP>C] sucrose permeability assay demonstrated that Sac-0601 was able to prevent VEGF-induced retinal endothelial permeability. The compound inhibited the vascular leakage in retina of mice intravitreally injected with VEGF. And it also significantly reduced the leakage in retina of diabetic retinopathy mice model. Taken together, our findings suggest the potential therapeutic usefulness of Sac-0601 for retinal vascular permeability diseases.</P>