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Search Results: 1 - 10 of 814 matches for " Kyoungho Suk "
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Inhibitors of Microglial Neurotoxicity: Focus on Natural Products
Dong Kug Choi,Sushruta Koppula,Kyoungho Suk
Molecules , 2011, DOI: 10.3390/molecules16021021
Abstract: Microglial cells play a dual role in the central nervous system as they have both neurotoxic and neuroprotective effects. Uncontrolled and excessive activation of microglia often contributes to inflammation-mediated neurodegeneration. Recently, much attention has been paid to therapeutic strategies aimed at inhibiting neurotoxic microglial activation. Pharmacological inhibitors of microglial activation are emerging as a result of such endeavors. In this review, natural products-based inhibitors of microglial activation will be reviewed. Potential neuroprotective activity of these compounds will also be discussed. Future works should focus on the discovery of novel drug targets that specifically mediate microglial neurotoxicity rather than neuroprotection. Development of new drugs based on these targets may require a better understanding of microglial biology and neuroinflammation at the molecular, cellular, and systems levels.
Activation of CD147 with Cyclophilin A Induces the Expression of IFITM1 through ERK and PI3K in THP-1 Cells
Ju-Young Kim,Ho Kim,Kyoungho Suk,Won-Ha Lee
Mediators of Inflammation , 2010, DOI: 10.1155/2010/821940
Abstract: CD147, as a receptor for Cyclophilins, is a multifunctional transmembrane glycoprotein. In order to identify genes that are induced by activation of CD147, THP-1 cells were stimulated with Cyclophilin A and differentially expressed genes were detected using PCR-based analysis. Interferon-induced transmembrane 1 (IFITM1) was detected to be induced and it was confirmed by RT-PCR and Western blot analysis. CD147-induced expression of IFITM1 was blocked by inhibitors of ERK, PI3K, or NF- B, but not by inhibitors of p38, JNK, or PKC. IFITM1 appears to mediate inflammatory activation of THP-1 cells since cross-linking of IFITM1 with specific monoclonal antibody against it induced the expression of proinflammatory mediators such as IL-8 and MMP-9. These data indicate that IFITM1 is one of the pro-inflammatory mediators that are induced by signaling initiated by the activation of CD147 in macrophages and activation of ERK, PI3K, and NF- B is required for the expression of IFITM1. 1. Introduction Interferon-induced transmembrane (IFITM/Mil/fragilis) proteins, originally described based on their expression after IFN treatment [1], belong to a superfamily that is characterized by the presence of two transmembrane domains and an intervening highly conserved intracellular loop. Over 30 members of this superfamily are known to be involved in antiviral defense, immune cell signaling, cell adhesion, oncogenesis, and germ cell maturation [2–6]. As the first identified member of this superfamily, IFITM1 (CD225) has been studied for its involvement in the inhibition of viral replication [7], promotion of cancer cell invasion [8], and expression in transformed cells as a cancer marker [9–12]. CD147 (EMMPRIN/basigin/HAb18G/neurothelin/M6/TCSF) has two immunoglobulin-like extracellular domains and a short (39 amino acids long) intracellular domain [13]. CD147 plays a critical role in many pathological and physiological processes in a variety of cell types such as cancer cells, leukocytes, fibroblasts, and endothelial cells [14–17]. Stimulation of CD147 in fibroblast and endothelial cells has been shown to facilitate tumor invasion, metastasis, and angiogenesis [17, 18]. On the other hand, stimulation of CD147 in leukocytes leads to the enhancement of a variety of inflammatory processes that are associated with atherosclerosis, lung injury, rheumatoid arthritis (RA), chronic liver disease, and heart failure [19–21]. Two members of cyclophilin family, cyclophilin A and B (CypA and CypB), can interact and stimulate CD147 [22, 23]. These cyclosporine binding proteins can be
Mild Hypothermia Attenuates Intercellular Adhesion Molecule-1 Induction via Activation of Extracellular Signal-Regulated Kinase-1/2 in a Focal Cerebral Ischemia Model
Jung Sook Choi,Jaechan Park,Kyoungho Suk,Cheil Moon,Yong-Ki Park,Hyung Soo Han
Stroke Research and Treatment , 2011, DOI: 10.4061/2011/846716
Abstract: Intercellular adhesion molecule-1 (ICAM-1) in cerebral vascular endothelium induced by ischemic insult triggers leukocyte infiltration and inflammatory reaction. We investigated the mechanism of hypothermic suppression of ICAM-1 in a model of focal cerebral ischemia. Rats underwent 2 hours of middle cerebral artery occlusion and were kept at 37°C or 33°C during occlusion and rewarmed to normal temperature immediately after reperfusion. Under hypothermic condition, robust activation of extracellular signal-regulated kinase-1/2 (ERK1/2) was observed in vascular endothelium of ischemic brain. Hypothermic suppression of ICAM-1 was reversed by ERK1/2 inhibition. Phosphorylation of signal transducer and activator of transcription 3 (STAT3) in ischemic vessel was attenuated by hypothermia. STAT3 inhibitor suppressed ICAM-1 production induced by stroke. ERK1/2 inhibition enhanced phosphorylation and DNA binding activity of STAT3 in hypothermic condition. In this study, we demonstrated that hypothermic suppression of ICAM-1 induction is mediated by enhanced ERK1/2 activation and subsequent attenuation of STAT3 action. 1. Introduction Intercellular adhesion molecule-1 (ICAM-1) is a member of the immunoglobulin superfamily and the principal ligand for leukocyte function-associated antigen-1 (LFA-1), a member of the integrin superfamily. ICAM-1/LFA-1 adhesion system assists leukocyte movement into the tissue. LFA-1-positive leukocytes are induced to adhere to ICAM-1-positive endothelial surface [1, 2], and then to pass through the basement membrane into the tissue [3, 4]. Many animal and human studies indicate that ICAM-1 is implicated in the pathogenesis of ischemic cardiovascular and cerebrovascular disorders [5–8]. Especially during reperfusion period of stroke, infiltrated leukocytes contribute to the secondary injury by producing toxic substances that damage the brain cells and disrupt the blood-brain barrier [9, 10]. Since ICAM-1 is an important factor of leukocyte infiltration and reperfusion injury in stroke, intervention of ICAM-1 induction has been a promising therapeutic strategy against stroke. The remarkable benefit of mild hypothermia in brain ischemia has long been recognized and remains one of the most powerful neuroprotective strategies in cerebral ischemia both experimentally and clinically [11]. Many studies indicate that inflammatory response contributes significantly to the secondary injury after ischemia [12, 13], and protection by mild hypothermia is associated with anti-inflammatory processes [14–16]. Even though there is considerable
Plasminogen activator inhibitor type 1 regulates microglial motility and phagocytic activity
Hyejin Jeon, Jong-Heon Kim, Jae-Hong Kim, Won-Ha Lee, Myung-Shik Lee, Kyoungho Suk
Journal of Neuroinflammation , 2012, DOI: 10.1186/1742-2094-9-149
Abstract: In this study, we identified PAI-1 in the culture medium of mouse mixed glial cells by liquid chromatography and tandem mass spectrometry. Secretion of PAI-1 from glial cultures was detected by ELISA and western blotting analysis. Cell migration was evaluated by in vitro scratch-wound healing assay or Boyden chamber assay and an in vivo stab wound injury model. Phagocytic activity was measured by uptake of zymosan particles.The levels of PAI-1 mRNA and protein expression were increased by lipopolysaccharide and interferon-γ stimulation in both microglia and astrocytes. PAI-1 promoted the migration of microglial cells in culture via the low-density lipoprotein receptor-related protein (LRP) 1/Janus kinase (JAK)/signal transducer and activator of transcription (STAT)1 axis. PAI-1 also increased microglial migration in vivo when injected into mouse brain. PAI-1-mediated microglial migration was independent of protease inhibition, because an R346A mutant of PAI-1 with impaired PA inhibitory activity also promoted microglial migration. Moreover, PAI-1 was able to modulate microglial phagocytic activity. PAI-1 inhibited microglial engulfment of zymosan particles in a vitronectin- and Toll-like receptor 2/6-dependent manner.Our results indicate that glia-derived PAI-1 may regulate microglial migration and phagocytosis in an autocrine or paracrine manner. This may have important implications in the regulation of brain microglial activities in health and disease.
On Interpolation Functions of the Generalized Twisted -Euler Polynomials
Park KyoungHo
Journal of Inequalities and Applications , 2009,
Abstract: The aim of this paper is to construct -adic twisted two-variable Euler-( , )- -functions, which interpolate generalized twisted ( , )-Euler polynomials at negative integers. In this paper, we treat twisted ( , )-Euler numbers and polynomials associated with -adic invariant integral on . We will construct two-variable twisted ( , )-Euler-zeta function and two-variable ( , )- -function in Complex -plane.
Time-dependent effects of hypothermia on microglial activation and migration
Jung-Wan Seo, Jong-Heon Kim, Jae-Hong Kim, Minchul Seo, Hyung Soo Han, Jaechan Park, Kyoungho Suk
Journal of Neuroinflammation , 2012, DOI: 10.1186/1742-2094-9-164
Abstract: Microglial cells in culture were subjected to mild (33?°C) or moderate (29?°C) hypothermic conditions before, during, or after lipopolysaccharide (LPS) or hypoxic stimulation, and the production of nitric oxide (NO), proinflammatory cytokines, reactive oxygen species, and neurotoxicity was evaluated. Effects of hypothermia on microglial migration were also determined in in vitro as well as in vivo settings.Early-, co-, and delayed-hypothermic treatments inhibited microglial production of inflammatory mediators to varying degrees: early treatment was the most efficient, and delayed treatment showed time-dependent effects. Delayed hypothermia also suppressed the mRNA levels of proinflammatory cytokines and iNOS, and attenuated microglial neurotoxicity in microglia-neuron co-cultures. Furthermore, delayed hypothermia reduced microglial migration in the Boyden chamber assay and wound healing assay. In a stab injury model, delayed local hypothermia reduced migration of microglia toward the injury site in the rat brain.Taken together, our results indicate that delayed hypothermia is sufficient to attenuate microglial activation and migration, and provide the basis of determining the optimal time window for therapeutic hypothermia. Delayed hypothermia may be neuroprotective by inhibiting microglia-mediated neuroinflammation, indicating the therapeutic potential of post-injury hypothermia for patients with brain damages exhibiting some of the inflammatory components.
Identities of Symmetry for Euler Polynomials Arising from Quotients of Fermionic Integrals Invariant under
Kim DaeSan,Park KyoungHo
Journal of Inequalities and Applications , 2010,
Abstract: We derive eight basic identities of symmetry in three variables related to Euler polynomials and alternating power sums. These and most of their corollaries are new, since there have been results only about identities of symmetry in two variables. These abundances of symmetries shed new light even on the existing identities so as to yield some further interesting ones. The derivations of identities are based on the -adic integral expression of the generating function for the Euler polynomials and the quotient of integrals that can be expressed as the exponential generating function for the alternating power sums.
Grassmann manifold Bosonization of QCD in Two Dimensions
KyoungHo Han,H. J. Shin
Mathematics , 1997, DOI: 10.1063/1.532081
Abstract: Two dimensional QCD is bosonized to be an integrably deformed Wess-Zumino-Witten model under proper limit. Fermions are identified having indices of the Grassmann manifold. Conditions for integrability are analyzed and their physical meanings are discussed. We also address the nature of the exactly solvable part of the theory and find the infinitely many conserved quantities.
On Some Arithmetical Properties of the Genocchi Numbers and Polynomials
Park KyoungHo,Kim Young-Hee
Advances in Difference Equations , 2008,
Abstract: We investigate the properties of the Genocchi functions and the Genocchi polynomials. We obtain the Fourier transform on the Genocchi function. We have the generating function of -Genocchi polynomials. We define the Cangul-Ozden-Simsek's type twisted -Genocchi polynomials and numbers. We also have the generalized twisted -Genocchi numbers attached to the Dirichlet's character . Finally, we define zeta functions related to -Genocchi polynomials and have the generating function of the generalized -Genocchi numbers attached to .
Composite Skyrme Model with Vector Mesons
Kwanghoon Hahm,KyoungHo Han,H. J. Shin
Physics , 1997, DOI: 10.1103/PhysRevD.56.1812
Abstract: We study the composite Skyrme model, proposed by Cheung and G\"{u}rsey, introducing vector mesons in a chiral Lagrangian. We calculate the static properties of baryons and compare with results obtained from models without vector mesons.
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