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Lee, Seung-Hee,Lee, Jee Hyun,Kim, Eun-Ju,Kim, Won-Jung,Suk, Kyoungho,Kim, Joo-Hwan,Song, Gyu Yong,Lee, Won-Ha Published for the International Federation for Cel 2012 Cell biology international Vol.36 No.7
<P>Decursin and related coumarin compounds in herbal extracts have a number of biological activities against inflammation, angiogenesis and cancer. We have analysed a derivative of decursin (CSL-32) for activity against inflammatory activation of cancer cells, such as migration, invasion and expression of pro-inflammatory mediators. The human fibrosarcoma cell line, HT1080, was treated with TNFα (tumour necrosis factor α) in the presence or absence of CSL-32. The cellular responses and modification of signalling adapters were analysed with respect to the production of pro-inflammatory mediators, as also migration, adhesion and invasion. Treatment of HT1080 cells with CSL-32 inhibited their proliferation, without affecting cell viability, and TNFα-induced expression of pro-inflammatory mediators, such as MMP-9 (matrix metalloproteinase-9) and IL-8 (interleukin-8). CSL-32 also suppressed phosphorylation and degradation of IκB (inhibitory κB), phosphorylation of p65 subunit of NF-κB (nuclear factor-κB) and nuclear translocation of NF-κB, which are required for the expression of pro-inflammatory mediators. In addition, CSL-32 inhibited invasion and migration of HT1080 cells, as also cellular adhesion to fibronectin, an ECM (extracellular matrix) protein. CSL-32 treatment resulted in a dose-dependent inhibition of PI3K (phosphoinositide 3-kinase) activity, required for the cellular migration. The analyses show that CSL-32 inhibits processes associated with inflammation, such as the production of pro-inflammatory mediators, as well as adhesion, migration and invasion in HT1080 cells.</P>
Lee, Sang‐,Min,Kim, Eun‐,Ju,Suk, Kyoungho,Lee, Won‐,Ha Blackwell Publishing Ltd 2011 Immunology Vol.134 No.2
<P><B>Summary</B></P><P>B‐cell activation factor of the tumour necrosis factor family (BAFF), an important regulator of B‐cell survival, has recently been found to be expressed on the surface of murine and human macrophages and engagement with its receptor was shown to trigger induction of pro‐inflammatory mediators and block phagocytic activity. In an effort to generate immunomodulatory agents that can regulate BAFF‐mediated signal, decapeptides representing the intracellular immunoreceptor tyrosine‐based inhibitory motifs (ITIMs) of immune receptor expressed on myeloid cells (IREM)‐1, an inhibitory transmembrane protein expressed on myeloid cells, were synthesized in conjugation with HIV‐transactivator of transcription (TAT)<SUB>48–57,</SUB> which facilitates the internalization of peptides into cells. Interestingly, all five of these synthetic peptides, representing the five ITIM‐like sequences present in the cytoplasmic tail of IREM‐1, exhibited inhibitory action against BAFF‐mediated induction of matrix metalloproteinase‐9 and interleukin‐8 expression. Inhibitor assay and immunoprecipitation assay followed by Western blotting demonstrated that the inhibitory action was mediated by Src homology 2 (SH2)‐containing tyrosine phosphatase (SHP)‐1 and/or phosphoinositide 3‐kinase (PI3K). ELISA‐based nuclear factor‐κB DNA binding assay observed that the synthetic peptides blocked the activation of nuclear factor‐κB in an SHP‐1 and phosphoinositide 3‐kinase‐dependent manner. Three of these synthetic peptides exhibited varying degrees of inhibitory action against BAFF‐mediated blockage of phagocytosis in a SHP‐1 and PI3K‐dependent manner. These data indicate that the synthetic peptides are capable of blocking BAFF‐mediated regulation of macrophage activities through the activation of SHP‐1 and PI3K as well as inhibition of nuclear factor‐κB activation.</P>
Kyoungho Lee,Hyun-Bae Lee,Hae-Kang Jung,Jae-Yoon Sim,Hong-June Park IEEE 2008 IEEE TRANSACTIONS ON ADVANCED PACKAGING Vol.31 No.4
<P>A serpentine guard trace is proposed to reduce the peak far-end crosstalk voltage and the crosstalk induced timing jitter of parallel microstrip lines on printed circuit boards. The vertical sections of the serpentine guard increase the mutual capacitance without much changing the mutual inductance between the aggressor and victim lines. This reduces the difference between the capacitive and inductive couplings and hence the far-end crosstalk. Comparison with the no guard, the conventional guard, and the via-stitch guard shows that the serpentine guard gives the smallest values in both the peak far-end crosstalk voltage and the timing jitter. The time domain reflectometer (TDR) measurement shows that the peak far-end crosstalk voltage of serpentine guard is reduced to 44% of that of no guard. The eye diagram measurement of pseudo random binary sequence (PRBS) data shows that the timing jitter is also reduced to 40% of that of no guard.</P>
Regulation by lipocalin‐2 of neuronal cell death, migration, and morphology
Lee, Shinrye,Lee, Won‐,Ha,Lee, Myung‐,Shik,Mori, Kiyoshi,Suk, Kyoungho Wiley Subscription Services, Inc., A Wiley Company 2012 JOURNAL OF NEUROSCIENCE RESEARCH - Vol.90 No.3
<P><B>Abstract</B></P><P>A secreted protein, lipocalin‐2 (LCN2), has been previously shown to regulate a variety of cellular phenotypes such as cell death, migration, and morphology. The role of LCN2, however, appears to be different depending on the cellular context. Here, we investigated how LCN2 influences neuronal phenotypes by using primary cortical neuronal cell cultures and neuroblastoma cell lines as a model. When exposed to LCN2 protein, neurons and neuroblastoma cells were sensitized to cell death evoked by nitric oxide, oxidative stress, and tumor necrosis factor‐α (TNF‐α). A forced expression of <I>lcn2</I> in glia enhanced neuronal cell death in cocultures of glia and neurons, indicating that both exogenous protein addition and endogenous expression of <I>lcn2</I> give rise to similar results. Iron and BCL2‐interacting mediator of cell death (BIM) protein were involved in LCN2‐induced cell death sensitization, based on the studies using iron donor, chelator, siderophore, and short hairpin RNA (shRNA)‐mediated knockdown of <I>bim</I> expression. Furthermore, cell migration assay and immunofluorescence microscopic observation revealed that LCN2 accelerated neuronal motility and process extension, suggesting multiple roles for LCN2 in the regulation of neuronal cell death, migration, and morphology. © 2011 Wiley Periodicals, Inc.</P>
Serpentine Microstrip Lines With Zero Far-End Crosstalk for Parallel High-Speed DRAM Interfaces
Kyoungho Lee,Hae-Kang Jung,Hyung-Joon Chi,Hye-Jung Kwon,Jae-Yoon Sim,Hong-June Park IEEE 2010 IEEE TRANSACTIONS ON ADVANCED PACKAGING Vol.33 No.2
<P>Serpentine microstrip lines are proposed to eliminate the far-end crosstalk in parallel high-speed interfaces by increasing the capacitive coupling ratio to equal the inductive coupling ratio. Zero far-end crosstalk voltage waveform and zero crosstalk-induced jitter (CIJ) were achieved on an FR4 printed circuit board, by adjusting the unit section length of the serpentine structure. Application of the proposed serpentine microstrip lines to the 2-drop stub series terminated logic DRAM channel increased the maximum data rate from 0.9 to 1.4 Gb/s and reduced CIJ by ~ 78 ps at 3.3 Gb/s.</P>
Lee, Min-Young,Kim, Won-Jung,Kang, Yoon-Joong,Jung, Young-Mi,Kang, Young-Mo,Suk, Kyoungho,Park, Jeong-Euy,Choi, Eun-Mi,Choi, Beom-Kyu,Kwon, Byoung S.,Lee, Won-Ha Federation of American Societies for Experimental 2006 Journal of Leukocyte Biology Vol.80 No.4
<P>Z39Ig is a transmembrane protein containing two Ig homology domains with unknown functions. Immunohistochemical analyses of human carotid atherosclerotic plaques detected Z39Ig staining in areas rich in foamy macrophages. Z39Ig staining was also observed in macrophages in the lining layers and sublining areas of rheumatoid arthritis synovium. Z39Ig staining in the osteoarthritis synovium was restricted to macrophages in the lining layers. To identify the role(s) of Z39Ig in the function of macrophages, we used human monocytic cell lines TF-1A (Z39Ig-negative) and THP-1 (Z39Ig-positive). The expression of Z39Ig was induced in TF-1A cells ,when they were differentiated into macrophages by treatment with PMA. The stimulation of PMA-treated TF-1A or THP-1 cells with immobilized anti-Z39Ig mAb induced the secretion of IL-8 and matrix metalloproteinase (MMP)-9, which was dependent on NF-kappaB activation. These data indicate that the macrophage Z39Ig is involved in the pathogenesis of inflammatory diseases through chemokine induction, which will promote the migration of inflammatory cells into the lesion area, and MMP-9 induction, which will contribute to cartilage destruction or extracellular matrix degradation.</P>
Macrophages express membrane bound form of APRIL that can generate immunomodulatory signals
Lee, Sang-Min,Jeon, Sung-Tak,Suk, Kyoungho,Lee, Won-Ha Blackwell Publishing Ltd 2010 Immunology Vol.131 No.3
<P>Summary</P><P>Members of the tumour necrosis factor superfamily play an essential role in inducing various biological responses including proliferation, differentiation, survival and cell death. A proliferation-inducing ligand (APRIL), first identified as a stimulant of tumour proliferation, is now known as a regulator of B-cell-mediated immune responses through the modulation of B-cell survival and activation. However, the role of APRIL in macrophage function has not been explored. High level expression of APRIL was detected on the surface of cells of the monocytic lineage including the human macrophage-like cell line, THP-1. To identify the role of APRIL in macrophage functions, THP-1 cells were stimulated with either its counterpart (TACI : Fc fusion protein) or a monoclonal antibody that is specific to APRIL. Stimulation of APRIL resulted in the expression of pro-inflammatory mediators such as interleukin-8 and matrix metalloproteinase-9 through the activation of mitogen-activated protein kinase and nuclear factor-&kgr;B. In contrast, stimulation of APRIL had an inhibitory effect on processes that require cytoskeletal movement such as phagocytosis of opsonized zymosan and chemotaxis through an inhibition of phosphatidylinositol 3-kinase activity. These observations demonstrate that macrophages express a membrane-bound form of APRIL which, upon stimulation, modulates the activities of macrophages through stimulation or inhibition of processes associated with inflammation.</P>