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Sun, Hu-Nan,Kim, Sun-Uk,Huang, Song Mei,Kim, Jin-Man,Park, Young-Ho,Kim, Seok-Ho,Yang, Hee-Young,Chung, Kyoung-Jin,Lee, Tae-Hoon,Choi, Hoon Sung,Min, Ju Sik,Park, Moon-Ki,Kim, Sang-Keun,Lee, Sang-Rae Blackwell Publishing Ltd 2010 Journal of Neurochemistry Vol.114 No.1
<P><I>J. Neurochem</I>. (2010) <B>114</B>, 39–50.</P><P>Abstract</P><P>Reactive oxygen species (ROS) actively participate in microglia-mediated pathogenesis as pro-inflammatory molecules. However, little is known about the involvement of specific antioxidants in maintaining the microglial oxidative balance. We demonstrate that microglial peroxiredoxin (Prx) 5 expression is up-regulated by lipopolysaccharide (LPS) through activation of the ROS-sensitive signaling pathway and is involved in attenuation of both microglial activation and nitric oxide (NO) generation. Unlike in stimulation of oxidative insults with paraquat and hydrogen peroxide, Prx V expression is highly sensitive to LPS-stimulation in microglia. Reduction of ROS level by treatment with either NADPH oxidase inhibitor or antioxidant ablates LPS-mediated Prx V up-regulation in BV-2 microglial cells and is closely associated with the activation of the c-<I>jun</I> N-terminal kinase (JNK) signaling pathway. This suggests the involvement of ROS/JNK signaling in LPS-mediated Prx V induction. Furthermore, NO induces Prx V up-regulation that is ablated by the addition of inducible nitric oxide synthase inhibitor or deleted mutation of inducible nitric oxide synthase in LPS-stimulated microglia. Therefore, these results suggest that Prx V is induced by cooperative action among the ROS, RNS, and JNK signaling cascades. Interestingly, knockdown of Prx V expression causes the acceleration of microglia activation, including augmented ROS generation and JNK-dependent NO production. In summary, we demonstrate that Prx V plays a key role in the microglial activation process through modulation of the balance between ROS/NO generation and the corresponding JNK cascade activation.</P>
Sun, Hu-Nan,Kim, Sun-Uk,Lee, Mi-Sook,Kim, Sang-Keun,Kim, Jin-Man,Yim, Mijung,Yu, Dae-Yeul,Lee, Dong-Seok Pharmaceutical Society of Japan 2008 Biological & pharmaceutical bulletin Vol.31 No.9
<P>The importance of microglial reactive oxygen species (ROS) signaling in neuroinflammatory processes has been well demonstrated; however, relatively little is known regarding the related mechanisms underlying these processes. Here, we show that ROS-dependent signal pathways that govern microglial phagocytosis are highly dependent upon nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox) activation. Specifically, phagocytosis was greatly reduced by both antioxidant and Nox inhibitor treatments in lipopolysaccharide (LPS)-stimulated BV-2 microglia. Additionally, there was a marked reduction in intracellular ROS content. These results suggest that Nox is the main ROS source for LPS-induced microglial phagocytosis. More decisive evidence for the involvement of ROS in phagocytosis was obtained from an examination of phosphatidyl inositol 3-kinase (PI3-K) and p38 mitogen-activated protein kinase (MAPK) signal pathway activation under reduced ROS levels. These two kinases were activated by LPS treatment and inhibited by ROS neutralization and Nox inhibition. We conclude that microglial phagocytosis requires ROS-dependent PI3-K and p38 MAPK activation and that Nox-derived ROS functions as an upstream regulator of both PI3-K and p38 MAPK. These findings will provide a fundamental basis for a therapeutic modality in inflammation-mediated neurodiseases.</P>
Sun Hu-Nan,Fang Wan,Jin Mei-Hua,Han Ying-Hao,Kim Sun-Uk,Lee Sang-Han,Kim Nam-Soon,Kim Cheol-Hee,Lee Dong-Seok The Korean Society for Biomedical Laboratory Scien 2004 Journal of biomedical laboratory sciences Vol.10 No.4
Inflammatory factor such as Interleukin-1 play important roles in determining the fate of both acute and chronic neurological disorders. We investigated whether inhibitors of PKC or PTK can serve as pharmacological agents to reduce IL-I production and the mechanisms underlying their pharmacological effects in a mixed population of glia. Inhibitors of PKC such as H7, Go6976 and Ro31-8220 significantly reduced both the mRNA and protein levels of IL-1α and IL-β in lipopolysaccharide-activated primary glial cells. While the PTK inhibitor genistein also significantly reduced the production of these cytokines, it did not affect the expression of their mRNA. Taken together, inhibitors of PKC and PTK could serve as pharmacological agents to reduce IL-1 production. However, the mechanisms underlying their pharmacological effects are different. Our results provide evidence that inhibitors of protein kinases can serve as pharmacological agents to modulate IL-1 production in glial cell, and in turn, alleviate neuronal injury.
Kim, Sun-Uk,Park, Young-Ho,Kim, Jin-Man,Sun, Hu-Nan,Song, In-Sung,Huang, Song Mei,Lee, Sang-Hee,Chae, Jung-Il,Hong, Su,Sik Choi, Sung,Choi, Seung-Cheol,Lee, Tae-Hoon,Kang, Sang Won,Rhee, Sue Goo,Chang AlphaMed Press 2014 Stem Cells Vol.32 No.4
<P>Redox balance has been suggested as an important determinant of 'stemness' in embryonic stem cells (ESCs). In this study, we demonstrate that peroxiredoxin (Prx) plays a pivotal role in maintenance of ESC stemness during neurogenesis through suppression of reactive oxygen species (ROS)-sensitive signaling. During neurogenesis, Prx I and Oct4 are expressed in a mutually dependent manner and their expression is abruptly downregulated by an excess of ROS. Thus, in Prx I(-/-) or Prx II(-/-) ESCs, rapid loss of stemness can occur due to spontaneous ROS overload, leading to their active commitment into neurons; however, stemness is restored by the addition of an antioxidant or an inhibitor of c-Jun N-terminal kinase (JNK). In addition, Prx I and Prx II appear to have a tight association with the mechanism underlying the protection of ESC stemness in developing teratomas. These results suggest that Prx functions as a protector of ESC stemness by opposing ROS/JNK cascades during neurogenesis. Therefore, our findings have important implications for understanding of maintenance of ESC stemness through involvement of antioxidant enzymes and may lead to development of an alternative stem cell-based therapeutic strategy for production of high-quality neurons in large quantity.</P>
Kim, Sun-Uk,Hwang, Chang Nam,Sun, Hu-Nan,Jin, Mei-Hua,Han, Ying-Hao,Lee, Hwang,Kim, Jin-Man,Kim, Sang-Keun,Yu, Dae-Yeul,Lee, Dong-Seok,Lee, Sang Ho Pharmaceutical Society of Japan 2008 Biological & pharmaceutical bulletin Vol.31 No.5
<P>Imbalance between oxidative stress and antioxidative defence system is generally known as one of mechanisms causing an oxidative stress-medieated neuropathogenesis. Peroxiredoxins (Prxs), a family of antioxidative enzymes neutralizing cellular hydroperoxides, was characterized recently, but their distributions and roles have not been resolved clearly or controversial in the central nervous system, Therefore, the present study was carried out to determine the specific cell types that express Prx I in the mouse brain and primary neural cells, and to examine its antioxidative role in the preferential cell types. Immunohistochemical reactivity for Prx I was detected dominantly in oligodendrocytes and rarely in microglia, whereas strong and specific immunoreactivity for Prx I was observed exclusively in microglia of primary neural cell culture. Further evidences for Prx I specificity were its relatively high expression in BV-2 microglial cells and its upregulated expression in microglia after lipopolysaccharide (LPS) stimulation. These results imply that Prx I can be used as an indicator of microglial activation. Inhibition of p38 MAPK ablated LPS-mediated Prx I upregulation and sensitized the microglia to H<SUB>2</SUB>O<SUB>2</SUB>-mediated cell death. These findings indicate that Prx I function as a scavenger for H<SUB>2</SUB>O<SUB>2</SUB> generated during microglial activation. The results of this study will help in unraveling the neuropathologic roles of the six Prx isoforms in neural function.</P>
Hu-Nan Sun,Wan Fang,Mei-Hua Jin,Ying-Hao Han,Sun-Uk Kim,Sang-Han Lee,Nam-Soon Kim,Cheol-Hee Kim,Dong-Seok Lee 대한의생명과학회 2004 Biomedical Science Letters Vol.10 No.4
Inflammatory factor such as Interleukin-1 play important roles in determining the fate of both acute and chronic neurological disorders. We investigated whether inhibitors of PKC or PTK can serve as pharmacological agents to reduce IL-1 production and the mechanisms underlying their pharmacological effects in a mixed population of glia. Inhibitors of PKC such as H7, G?6976 and Ro31-8220 significantly reduced both the mRNA and protein levels of IL-1α and IL-β in lipopolysaccharide-activated primary glial cells. While the PTK inhibitor genistein also significantly reduced the production of these cytokines, it did not affect the expression of their mRNA. Taken together, inhibitors of PKC and PTK could serve as pharmacological agents to reduce IL-1 production. However, the mechanisms underlying their pharmacological effects are different. Our results provide evidence that inhibitors of protein kinases can serve as pharmacological agents to modulate IL-1 production in glial cell, and in tum, alleviate neuronal injury.
Kim, Sun-Mi,Lee, Kie-Jin,Bae, Myung-Ho,Lee, Hu-Jong,Cha, Deok-Joon,Takayuki Ishibashi,Katsuaki Sato,Kim, Jin-Tae The Korean Superconductivity Society 2003 Progress in superconductivity Vol.4 No.2
We have measured the transport properties of $Bi_2$$Sr_2$$CaCu_2$$O_{8+d}$ (BSCCO) intrinsic Josephson junction mesa. Transport measurements with current flow along the c-axis, perpendicular to the layer of mesa showed multi-branch structures on the current-voltage characteristics. For single intrinsic junctions, the microwave radiation appears in the form of three different modes of oscillations, which include Josephson emission, nonequilibrium broad emission and sharp coherent microwave emission. Mutual phase interactions between two-mesas structures of BSCCO intrinsic Josephson junctions were studied. The results were explained within the framework of the Josephson plasma excitation model due to quasiparticle injection.n.