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Bae, Sang-Cheol,Kim, Jinseok,Choe, Jung-Yoon,Park, Won,Lee, Sang-Heon,Park, Yong-Beom,Shim, Seung-Cheol,Lee, Shin-Seok,Sung, Yoon-Kyoung,Choi, Chan-Bum,Lee, So-Ra,Park, HanYu,Ahn, Yongho H. K. Lewis 2017 Annals of the rheumatic diseases Vol.76 No.1
<P>Conclusion The study met the primary objective of demonstrating equivalent efficacy of HD203 and ETN. HD203 was well tolerated, with safety comparable with ETN in this population of patients with RA.</P>
Network Analysis을 이용한 류마티스관절염 활액 대식세포에서 유전자 발현 연구
지종대 ( Jong Dae Ji ),김태환 ( Tae Hwan Kim ),이빛나라 ( Bit Na Ra Lee ),최성재 ( Sung Jae Choi ),이영호 ( Young Ho Lee ),송관규 ( Gwan Gyu Song ) 대한류마티스학회 2011 대한류마티스학회지 Vol.18 No.2
Objective. We wanted to investigate the mechanisms that could account for the pathogenesis of rheumatoid arthritis, so we examined the different expressions of the genes in rheumatoid arthritis (RA) synovial fluid macrophages as compared with that of normal peripheral blood (PB) monocyte-derived macrophages using microarray and bioinformatic analysis. Methods. We examined the expression of genes by using a gene expression oligonucleotide microarray. The differences of the gene expressions between the RA synovial macrophages and the normal PB monocytes-derived macrophages were analyzed using bioinformatic tools, including cytoscape and its plugin. Results. In this study, we found that 899 genes (464 genes up-regulated and 435 genes down-regulated) were differentially expressed between the two groups. Among the 899 genes, 552 genes were included for gene ontology analysis and network analysis. Based on biological process ontology, they were categorised mainly into immune response processes, responses to stimulus and signaling and regulation of biological processes. In addition to the genes related with STAT1 and AP-1 signaling, we found that the genes involved in the antigen processing and the cell cycle are abundantly expressed in RA synovial macrophages, suggesting that these genes may play an important role in the pathogenesis of RA. Conclusion. Our study suggest that this approach using integration of the gene expression profile with the protein interaction data may help to find several important pathogenic mechanisms in RA.
Ra Sang Hyun,Chang Euijin,Kwon Ji-Soo,Kim Ji Yeun,Son JuYeon,Kim Woori,Jang Choi Young,Jang Hyeon Mu,Bae Seongman,Jung Jiwon,Kim Min Jae,Chong Yong Pil,Lee Sang-Oh,Choi Sang-Ho,Kim Yang Soo,Lee Keun H 대한의학회 2024 Journal of Korean medical science Vol.39 No.35
Background: The pathophysiological mechanisms underlying the post-acute sequelae of severe acute respiratory syndrome coronavirus 2 infection (PASC) are not well understood. Our study aimed to investigate various aspects of theses mechanisms, including viral persistence, immunological responses, and laboratory parameters in patients with and without PASC. Methods: We prospectively enrolled adults aged ≥ 18 years diagnosed with coronavirus disease 2019 (COVID-19) between August 2022 and July 2023. Blood samples were collected at three time-points: within one month of diagnosis (acute phase) and at 1 month, and 3 months post-diagnosis. Following a recent well-designed definition of PASC, PASC patients were defined as those with a questionnaire-based PASC score ≥ 12 persisting for at least 4 weeks after the initial COVID-19 diagnosis. Results: Of 57 eligible COVID-19 patients, 29 (51%) had PASC, and 28 (49%) did not. The PASC group had significantly higher nucleocapsid protein (NP) antigenemia 3 months after COVID-19 diagnosis (P = 0.022). Furthermore, several cytokines, including IL-2, IL-17A, VEGF, RANTES, sCD40L, IP-10, I-TAC, and granzyme A, were markedly elevated in the PASC group 1 and/or 3 month(s) after COVID-19 diagnosis. In contrast, the median values of several serological markers, including thyroid markers, autoimmune indicators, and stress-related hormones, were within the normal range. Conclusion: Levels of NP antigen and of various cytokines involved in immune responses become significantly elevated over time after COVID-19 diagnosis in PASC patients compared to non-PASC patients. This suggests that PASC is associated with prolonged immune dysregulation resulting from heightened antigenic stimulation.
Lee, So-Ra,Lee, Hyo-Eun,Kang, Yun Ok,Hwang, Wan-Seok,Choi, Seong-Ho Hindawi Limited 2014 Advances In Materials Science And Engineering Vol.2014 No.-
<P>Bienzymatic<I>acetylcholinesterase</I>(AChE) and<I>choline oxidase</I>(ChOx) immobilized biosensor based on a phenyl carboxylic acid-grafted multiwalled carbon nanotube (MWNT) modified glass carbon electrode (GCE) and carbon-screen printed electrode (SPE) was fabricated for acetylcholine detection in human blood samples. Phenyl carboxylic acid-modified MWNT supports were prepared by electrochemical polymerization of 4-carboxyphenyl diazonium salts, which were synthesized by an amine group and sodium nitrite, on the surface of the MWNT-modified GCE and SPE in 0.1 M PBS. The successful fabrication of the AChE-ChOx-immobilized biosensor was confirmed via scanning electron microscopy (SEM), X-ray photoelectron spectroscopy (XPS), electrochemical impedance spectroscopy (EIS), and cyclic voltammetry (CV). The sensing range of the biosensor based on a GCE and SPE was 1.0~10 <I>μ</I>M and 10~100 <I>μ</I>M, respectively. The interfering effect of 0.1 M L-ascorbic acid, 0.1 M L-cysteine, and 0.1 M uric acid to 0.1 M acetylcholine was 3.00%, 9.00%, and 3.00%, respectively. Acetylcholine in a human blood sample was detected by the AChE-ChOx-immobilized biosensor.</P>
Lee, Song-Yi,Lee, Yong-Gyu,Byeon, Se-Eun,Han, So-Ryu,Choi, Sun-Shim,Kim, Ae-Ra,Lee, Jae-Hwi,Lee, Sang-Jin,Hong, Sung-Youl,Cho, Jae-Youl 대한약학회 2010 Archives of Pharmacal Research Vol.33 No.11
Sparassis crispa (SC) is an edible mushroom that harbours ${\beta}$-glucans reported to possess immunostimulatory and anticancer properties. The role of SC in regulating the functional activation of macrophages is yet to be fully elucidated. The objective of this study was to investigate the molecular mechanism underlying the immune-stimulatory function of Sparassis crispa soluble ${\beta}$-glucan (Sc-SG) on macrophages. According to this study, Sc-SG was able to stimulate nitric oxide (NO) production as well as enhance the expression of inducible NO synthase (iNOS) from macrophage-like RAW264.7 cells. NO production was strongly suppressed by mitogen-activated protein kinase (MAPK) inhibitors such as U0126, extracellular signalregulated kinase, SB203580, a p38 inhibitor, and SP600125, a c-Jun N-terminal kinase inhibitor. Thus, indicating that Sc-SG-induced NO release is possibly mediated by MAPK. Sc-SG induced phosphorylation of extracellular signal-regulated kinase, p38, and JNK in a timedependent manner. Moreover, Sc-SG triggered the phosphorylation and translocation of c-Jun and c-Fos, components of the transcription factor AP-1, activated by MAPK. The results of this study suggest that MAPK may be a major signaling enzyme that regulates the Sc-SG-mediated NO production in macrophages.
CNBP acts as a key transcriptional regulator of sustained expression of interleukin-6
Lee, Eunhye,Lee, Taeyun A.,Kim, Ji Hyun,Park, Areum,Ra, Eun A.,Kang, Sujin,Choi, Hyun jin,Choi, Junhee L.,Huh, Hyunbin D.,Lee, Ji Eun,Lee, Sungwook,Park, Boyoun Oxford University Press 2017 Nucleic acids research Vol.45 No.6
<P><B>Abstract</B></P><P>The transcription of inflammatory genes is an essential step in host defense activation. Here, we show that cellular nucleic acid-binding protein (CNBP) acts as a transcription regulator that is required for activating the innate immune response. We identified specific CNBP-binding motifs present in the promoter region of sustained inflammatory cytokines, thus, directly inducing the expression of target genes. In particular, lipopolysaccharide (LPS) induced <I>cnbp</I> expression through an NF-κB-dependent manner and a positive autoregulatory mechanism, which enables prolonged <I>il-6</I> gene expression. This event depends strictly on LPS-induced CNBP nuclear translocation through phosphorylation-mediated dimerization. Consequently, <I>cnbp</I>-depleted zebrafish are highly susceptible to <I>Shigella flexneri</I> infection <I>in vivo</I>. Collectively, these observations identify CNBP as a key transcriptional regulator required for activating and maintaining the immune response.</P>
Lee, Se-Ra,Mun, Jeong-Yeon,Jeong, Mi-So,Lee, Hyun-Hee,Roh, Yun-Gil,Kim, Won-Tae,Kim, Min-Hye,Heo, Jeonghoon,Choi, Yung Hyun,Kim, Su Jin,Cha, Hee-Jae,Jun, Mira,Leem, Sun-Hee MDPI AG 2019 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.20 No.11
<P>Tristetraprolin (TTP), a well-characterized AU-rich element (ARE) binding protein, functions as a tumor suppressor gene. The purpose of this study was to investigate whether a bioactive substance derived from a natural medicinal plant affects the induction of TTP and to elucidate its mechanism. We examined the effects of natural bioactive materials including Resveratrol (RSV), thymoquinone (TQ) and curcumin on the expression of TTP in cancer cell. TQ derived from a natural plant Nigella sativa increased the expression levels of TTP mRNA and proteins in a dose-dependent manner in gastric and breast cancer cells. TQ-induced TTP increased the instability of MUC4 mRNA by direct binding of TTP to ARE in the 3′UTR of MUC4 mRNA. The induction of TTP by TQ also reduced the proliferation, migration and invasion of cancer cells. The expression of the epithelial-mesenchymal (EMT)-related genes, which were target genes of TTP, was also decreased by the TQ treatment. In the in vivo experiments using mouse melanoma cells, TQ-induced TTP inhibited metastasis of tumor cells. We have found that TQ-induced TTP might inhibit metastasis by reducing tumor cell migration and invasion through destabilization of MUC4 mRNA, which suggest the MUC4 as a novel target to TTP.</P>
Lee, Byung-Hwan,Choi, Sun-Hye,Pyo, Mi Kyung,Shin, Tae-Joon,Hwang, Sung-Hee,Kim, Bo-Ra,Lee, Sang-MoK,Lee, Jun-Ho,Lee, Joon-Hee,Lee, Hui Sun,Choe, Han,Han, Kyou-Hoon,Kim, Hyoung-Chun,Rhim, Hyewhon,Yong, Springer-Verlag 2009 Molecules and cells Vol.27 No.5
<P>Nicotinic acetylcholine receptors (nAChRs) play important roles in nervous system functions and are involved in a variety of diseases. We previously demonstrated that ginsenosides, the active ingredients of Panax ginseng, inhibit subsets of nAChR channel currents, but not alpha7, expressed in Xenopus laevis oocytes. Mutation of the highly conserved Leu247 to Thr247 in the transmembrane domain 2 (TM2) channel pore region of alpha7 nAChR induces alterations in channel gating properties and converts alpha7 nAChR antagonists into agonists. In the present study, we assessed how point mutations in the Leu247 residue leading to various amino acids affect 20(S)-ginsenoside Rg(3) (Rg(3)) activity against the alpha7 nAChR. Mutation of L247 to L247A, L247D, L247E, L247I, L247S, and L247T, but not L247K, rendered mutant receptors sensitive to Rg(3). We further characterized Rg(3) regulation of L247T receptors. We found that Rg(3) inhibition of mutant alpha7 nAChR channel currents was reversible and concentration-dependent. Rg(3) inhibition was strongly voltage-dependent and noncompetitive manner. These results indicate that the interaction between Rg(3) and mutant receptors might differ from its interaction with the wild-type receptor. To identify differences in Rg(3) interactions between wild-type and L247T receptors, we utilized docked modeling. This modeling revealed that Rg(3) forms hydrogen bonds with amino acids, such as Ser240 of subunit I and Thr244 of subunit II and V at the channel pore, whereas Rg(3) localizes at the interface of the two wild-type receptor subunits. These results indicate that mutation of Leu247 to Thr247 induces conformational changes in the wild-type receptor and provides a binding pocket for Rg(3) at the channel pore.</P>