Biomedical subjects

Soo-Cheon Chae

Publications and source records attributed to Soo-Cheon Chae.

At least 19 recordsLinked to original sources

PubMed2006

Construction of a bacterial artificial chromosome library and characterization of hrp/hrc gene cluster of Pseudomonas syringae pathovar tagetis LMG5090.

Pseudomonas syringae pv. tagetis causes apical chlorosis of several plant species in the Asteraceae, including marigold. As a means to facilitate the isolation of pathogenicity genes and to characterize the genome of this bacterium, we have constructed a bacterial artificial chromosome library of P. syringae pv. tagetis strain LMG5090. The library consists of 1,536 clones with insert size ranging from 30 to 160 kb and an average size of 86 kb. Based upon colony hybridization, the BAC clone 420E23 containing the hrp/hrc gene cluster encoding the type III secretion system was identified from this library and subsequently shotgun sequenced. The hrp/hrc gene cluster of P. syringae pv. tagetis has a 23 kb sequence which contains 27 open reading frames. Comparative analysis of the hrp/hrc gene cluster of P. syringae pv. tagetis LMG5090, P. syringae pv. tomato DC3000, P. syringae pv. syringae B728a, and P. syringae pv. phaseolicola 1448A revealed that the entire hrp/hrc gene cluster of P. syringae pv. tagetis is conserved and identically arranged in all four pathovars.

Bacterial Outer Membrane Proteins↗

PubMed2006

Identification of single nucleotide polymorphisms in FOXJ1 and their association with allergic rhinitis.

Forkhead-box J1 (FOXJ1) is a presumed transcription factor that can suppress T cell activity, at least partially, through the repression of NFkappaB activity. Thus, dysregulation of FOXJ1 is thought to be associated with autoimmune diseases and/or other inflammatory diseases. To investigate the association between single nucleotide polymorphisms (SNPs) of human FOXJ1 and allergic rhinitis, we scanned the whole human FOXJ1 gene, including the promoter region, by direct sequencing of DNA from 32 individuals. We identified seven SNPs, three of which (g.-460C>T, g.1805G>T, and g.3375G>C) were chosen for large sample size genotyping (n=713), and to assess the genotype frequencies of these SNPs between controls and allergic rhinitis patients. We also investigated the relationships of each genotype with serum total IgE levels in allergic rhinitis patients, and compared the frequencies of haplotypes constructed by these SNPs between the two groups. Our results suggest that the SNPs g.-460C>T, g.1805G>T and g.3375G>C in the human FOXJ1 gene might be associated with susceptibility to allergic rhinitis (P=0.0184, 0.0076, and 0.0143, respectively). The main haplotype, CGG, also revealed a significant association with allergic rhinitis (P=0.000018). However, no significant association was found between serum total IgE levels and the genotypes of these polymorphisms.

Adult↗

PubMed2006

Identification of crystallin family proteins in vitreous body in rat endotoxin-induced uveitis: Involvement of crystallin truncation in uveitis pathogenesis.

Endotoxin-induced uveitis (EIU) is an animal model of acute ocular inflammation. To characterize the mechanism of EIU, we analyzed the infiltration of proteins in the vitreous bodies of rats with EIU and normal rats using 2-DE and micro LC/LC-MS/MS. Twenty spots were identified in vitreous bodies of rats. Eighteen of these spots were members of the crystallin family. The truncated form of beta A4- and beta B2-crystallin were predominant in normal vitreous bodies, but there were intact form of crystallins in lipopolysaccharide-injected rats with EIU. These results suggest that crystallin family proteins are the major group of proteins involved in uveitic vitreous and that C-terminal truncation of beta-crystallins may play a role in EIU-related disease progression.

Amino Acid Sequence↗

PubMed2005

Eotaxin-3 gene polymorphisms are associated with rheumatoid arthritis in a Korean population.

The eotaxin gene family (eotaxin, eotaxin-2, and eotaxin-3) has been implicated in the recruitment of eosinophils, basophiles and Th2 lymphocytes that is a central aspect of allergic diseases. We previously suggested that Eo2+179T>C and Eo2+275C>T of the eotaxin-2, and Eo3+2497T>G of the eotaxin-3 were significantly associated with susceptibility to asthma. To precisely determine whether these single nucleotide polymorphisms (SNPs) are associated with susceptibility to autoimmune disease such as rheumatoid arthritis (RA) in Koreans, we analyzed the genotype and allele frequencies for four SNPs (Eo2+179T>C, Eo2+275C>T, Eo2+304A>C, and Eo2+1272A>G) of the eotaxin-2, and three SNPs (Eo3+77C>T, Eo3+1577G>A, and Eo3+2497T>G) of the eotaxin-3 by single-base extension method. Although the genotype and allele frequencies of the eotaxin-2 SNPs gene between patients with RA and controls were not significantly different, the genotype and allele frequencies of the eotaxin-3SNPs between them were significantly associated. The genotype frequencies of Eo3+1577G>A and Eo3+2497T>G in patients with RA were significantly different from those in the controls (p = 0.0001 and p < 0.0001, respectively). Our results strongly suggest that the polymorphisms of eotaxin-3 might be associated with susceptibility to RA.

Adult↗

PubMed2004

The suggestive association of eotaxin-2 and eotaxin-3 gene polymorphisms in Korean population with allergic rhinitis.

The eotaxin gene family (eotaxin, eotaxin-2 and eotaxin-3) has been implicated in the recruitment of eosinophils, basophiles and Th2 lymphocytes that are central aspects of allergic diseases. To determine whether single-nucleotide polymorphisms (SNPs) of the eotaxin-2 and eotaxin-3 genes are associated with susceptibility to allergic rhinitis, we scanned 178 allergic rhinitis patients and 281 controls without allergic rhinitis using the direct sequencing and single-base extension (SBE) methods. We also calculated the haplotype frequencies between +179T>C and +275C>T of eotaxin-2 and +2497T>G of eotaxin-3 in both controls and allergic rhinitis patients. The haplotype frequency between controls and allergic rhinitis patients was suggestively associated (P=0.0001). The genotype frequencies of eotaxin-3 +2497T>G in allergic rhinitis patients were suggestively different from those in non-allergic rhinitis controls (P=<0.0007). Our results strongly suggest that the SNP of eotaxin-3 might be associated with susceptibility to allergic rhinitis.

Chemokine CCL24↗

PubMed2004

The polymorphisms of Tim-1 promoter region are associated with rheumatoid arthritis in a Korean population.

It has been determined that the family of T-cell immunoglobulin domain and mucin domain (TIM) proteins is expressed on T cells. A member of the TIM family, TIM-1, is considered to be a membrane protein associated with the development of Th2-biased immune responses and selectively expressed on Th2 cells. We previously showed that the exon 4 variations of Tim-1 are associated with susceptibility to allergic diseases, as well as autoimmune diseases such as rheumatoid arthritis (RA). In this study, we assessed the association between genotype and allele frequencies of the Tim-1 gene promoter region, in both RA patients and the controls without RA, using polymerase chain reaction-restriction fragment length polymorphism and single-base extension methods. We further investigated the relationships among the genotypes of each polymorphism and C-reactive protein or rheumatoid factor levels in RA patients. The genotype and allele frequencies of the -1637A>G polymorphism in RA patients are significantly different from those in the non-RA controls (P=0.0004 and P=0.001, respectively). Our results strongly suggest that polymorphism in the Tim-1 promoter region might be associated with susceptibility to RA.

Adult↗

PubMed2004

The polymorphisms of Th1 cell surface gene Tim-3 are associated in a Korean population with rheumatoid arthritis.

The family of T-cell immunoglobulin domain and mucin domain (TIM) proteins is identified to be expressed on T cells. A member of TIM family, TIM-3 is selectively expressed on the surface of differentiated Th1 cells. TIM-3 might have an important role in the induction of autoimmune diseases by regulating macrophage activation and interacts with TIM-3 ligand to regulate Th1 responses. In the present study, we analyzed the association of the genotype and allele frequencies between rheumatoid arthritis (RA) patients and the controls without RA using large samples size at the -1516G>T, -574T>G and 4259G>T polymorphic sites of human Tim-3 gene. We further investigated the relationships between the genotypes of each single nucleotide polymorphisms (SNPs) and C-reactive protein (CRP) or rheumatoid factor (RF) levels in RA patients. The genotype and allele frequencies of the -574T>G (P = 0.001 and 0.001, respectively) as well as the 4259G>T (P = 0.001 ands 0.003, respectively) between RA patients and non-RA controls were significantly different. These results strongly suggest that -574T>G and 4259G>T polymorphism of the Tim-3 might be associated with susceptibility to RA.

Adult↗

PubMed2004

3-Hydroxyanthranilic acid, one of metabolites of tryptophan via indoleamine 2,3-dioxygenase pathway, suppresses inducible nitric oxide synthase expression by enhancing heme oxygenase-1 expression.

Inducible nitric oxide (NO) synthase (iNOS), heme oxygenase (HO)-1, and indoleamine 2,3-dioxygenase (IDO) are simultaneously expressed in murine macrophages stimulated with interferon (IFN)-gamma and lipopolysaccharide (LPS). NO produced by iNOS suppresses IDO expression and also induces HO-1 expression. The antioxidant 3-hydroxyanthranilic acid (HA), one of metabolites of tryptophan via IDO pathway, has been previously reported to suppress iNOS expression. Because HO-1 expression can suppress iNOS expression, we investigated whether HA could suppress iNOS expression by affecting HO-1 expression in murine RAW 264.7 macrophages stimulated with IFN-gamma plus LPS. Treatment with exogenous HA dose-dependently suppressed iNOS expression and coincidently enhanced HO-1 expression. This suppressive effect of HA on iNOS expression was reversed by blocking HO-1 activity, and proven to be due to carbon monoxide (CO) produced by HO-1. In addition, either blocking of iNOS activity or addition of exogenous CO further enhanced IDO expression and activity. These results show for the first time that HA is able to suppress iNOS expression by enhancing HO-1 expression, thereby resulting in further increases in IDO expression and activity.

3-Hydroxyanthranilic Acid↗

PubMed2004

Analysis of the polymorphisms in eotaxin gene family and their association with asthma, IgE, and eosinophil.

The eotaxin gene family (eotaxin, eotaxin-2, and eotaxin-3) has been implicated in the recruitment of eosinophils, basophiles, and Th2 lymphocytes that is a central aspect of allergic diseases such as asthma. To determine whether the single nucleotide polymorphisms (SNPs) of eotaxin gene family are associated with susceptibility to asthma, we scanned 225 asthma patients and 294 non-asthmatic controls using the direct sequencing method. We further investigated the relationships among each SNP, eosinophils, and serum total IgE levels in asthma patients. Eleven SNPs were identified in the eotaxin gene family. We found that EoB179T > C (P = 0.0001), EoB275C > T (P = 0.018) of the eotaxin-2 and EoA2497T > G (P = 0.003) of the eotaxin-3 were significantly associated with the susceptibility of asthma. Furthermore, our data demonstrated for the first time that EoA2497T > G (P = 0.005) is related to serum total IgE level while EoA77C > T (P = 0.035) and EoA2497T > G (P = 0.033) are related to the peripheral blood eosinophil counts in asthma. Our results suggest that the polymorphisms of the eotaxin gene family are associated with the susceptibility of asthma and Eotaxin-3 might play the critical role for the recruitment of eosinophils and the maintenance of IgE levels.

Adult↗

PubMed2004

Molecular variations in Th1-specific cell surface gene Tim-3.

The family of T-cell immunoglobulin domain and mucin domain (TIM) proteins is identified to be expressed on T cells. A member of Tim family, Tim-3 (T cell immunoglobulin mucin 3) is selectively expressed on the surface of differentiated Th1 cells. Tim-3 might have an important role in the induction of autoimmune diseases by regulating macrophage activation and interacts with Tim-3 ligand to regulate Th1 responses. To determine the variation sites in the coding and promoter region of human Tim-3 gene, we performed variation scanning by direct sequencing using the genomic DNA isolated from the patients with asthma or allergic rhinitis and healthy controls without asthma and allergic rhinitis. We identified four single nucleotide polymorphisms (SNPs) including one novel SNPs (-1541C>T) and two variation sites (-1292_-1289delTAAA and -1282_-1278dupTAAAA) in the coding and promoter region of human Tim-3 gene in both the patients and healthy groups.

Asthma↗

PubMed2004

Carbon monoxide produced by heme oxygenase-1 suppresses T cell proliferation via inhibition of IL-2 production.

Heme oxygenase-1 (HO-1) catabolizes heme into CO, biliverdin, and free iron and serves as a protective enzyme by virtue of its anti-inflammatory, antiapoptotic, and antiproliferative actions. Previously, we have demonstrated that human CD4(+) T cells express HO-1 and that HO-1-overexpressing Jurkat T cells tend to display lower proliferative response. The aim of this study is to elucidate the mechanism(s) by which HO-1 can mediate its antiproliferative effect on CD4(+) T cells. Among the three HO-1 byproducts, only CO showed suppressive effect on T cell proliferation in response to anti-CD3 plus anti-CD28 Abs, mimicking the antiproliferative action of HO-1. CO blocked the cell cycle entry of T cells, which was independent of the guanylate cyclase/cGMP pathway. CO also suppressed the secretion of IL-2, and this suppressive effect of CO on IL-2 secretion mediated the antiproliferative action of CO. CO selectively inhibited the extracellular signal-regulated kinase pathway, which could explain the suppressive effects of CO on T cell proliferation and IL-2 secretion. Based on these findings, we suggest that HO-1/CO suppresses T cell proliferation and IL-2 secretion, possibly via its inhibition of extracellular signal-regulated kinase activation.

CD4-Positive T-Lymphocytes↗

PubMed2004

The exon 4 variations of Tim-1 gene are associated with rheumatoid arthritis in a Korean population.

The family of T-cell immunoglobulin domain and mucin domain (TIM) proteins is identified to be expressed on T cells. A member of Tim family, TIM-1, is considered as a membrane protein that is associated with the development of Th2 biased immune responses and selectively expressed on Th2 cells. In the present study, we analyzed the association of genotype and allele frequencies between rheumatoid arthritis (RA) patients and the controls without RA using large samples size at 5383_5397del and 5509_5511delCAA variations of Tim-1 gene. We further investigated the relationships among these variations to C-reactive protein (CRP) and rheumatoid factor (RF) levels in RA patients. Although these factors were not associated with exon 4 variations in RA patients, the genotype and allele frequencies of 5383_5397del variation site (P = 0.015 and 0.014, respectively) as well as 5509_5511delCAA variation site (P = 0.0002 and 0.0001, respectively) in RA patients were significantly different from those in the non-RA controls. Our results strongly suggest that the variations of Tim-1 exon 4 might be associated with the susceptibility to RA.

Adult↗

PubMed2004

Soluble oligomeric Abeta disrupts the protein kinase C signaling pathway.

Alzheimer's disease (AD) is characterized by selective neurodegeneration of neurons involved in cognitive function. Current hypothesis for AD etiology needs to be reconsidered because fibrillar Abeta cannot explain selective neurodegeneration. Recent evidence suggests oligomeric Abeta may be more relevant to AD etiology. Here we show signaling disruption induced by oligomeric Abeta. Using the MTT assay, NT2 showed greatest susceptibility to soluble oligomeric Abeta. In the kinase assay, treatment with either monomeric Abeta or fibrillar Abeta evoked no response in PKA, PKC and TK. Oligomeric Abeta treatment, however, inactivated membranous PKC but activated cytosolic PKC in NT2 within 24 h. Our data suggest that oligomeric Abeta may cause selective neurodegeneration through a PKC signaling, distinctive from fibrillar Abeta.

Amyloid beta-Peptides↗

PubMed2004

The association of TIM-3 gene polymorphism with atopic disease in Korean population.

The family of T-cell immunoglobulin domain and mucin domain (TIM) proteins is identified to be expressed on T cells. A member of the TIM family, TIM-3 is selectively expressed on the surface of differentiated T helper 1 (Th1) cells. TIM-3 might have an important role in the induction of autoimmune diseases by regulating macrophage activation and interacts with the TIM-3 ligand to regulate Th1 responses. In the present study, we analyzed the association of the genotype and allele frequencies between asthma or allergic rhinitis patients and nonatopic controls using large samples size at -1516G > T, -574T > G, and 4259G > T polymorphic sites of the Tim-3 gene. The genotype and allele frequencies of -574T > G polymorphism in asthma patients (p = 0.042 and p = 0.017, respectively) as well as allergic rhinitis patients (p = 0.008 and p = 0.003, respectively) were significantly different from those of nonatopic controls. Furthermore, the allele frequency of 4259G > T polymorphism in allergic rhinitis patients (p = 0.029) was also significantly different. Our results strongly suggest that the -574T > G polymorphism of Tim-3 might be associated with the susceptibility of atopic diseases such as asthma and allergic rhinitis.

Adult↗

PubMed2003

The association of the exon 4 variations of Tim-1 gene with allergic diseases in a Korean population.

The family of T-cell immunoglobulin domain and mucin domain (TIM) proteins is identified to be expressed on T cells. A member of Tim family, TIM-1, is considered as a membrane protein that is associated with the development of Th2 biased immune responses and may be selectively expressed on Th2 cells. In the present study, we analyzed the association of allele and genotype frequencies between asthma or atopy patients and the controls without asthma and atopy using large sample size at 5383_5397del and 5509_5511delCAA variations of Tim-1 gene. Although the allele frequency of 5509_5511delCAA variation in asthma was not significantly different (P=0.085), the genotype of 5509_5511delCAA variation in asthma was significantly associated with the susceptibility to asthma (P=0.037). The genotype and allele frequencies of 5383_5397del variation in atopic dermatitis were significantly different from those in the non-asthmatic and non-atopic controls (P=0.005 and P=0.002, respectively). Our results strongly suggest that the 5383_5397del variation site of Tim-1 exon 4 might be associated with atopic dermatitis susceptibility.

Asthma↗

PubMed2003

Differential expressions of heme oxygenase-1 gene in CD25- and CD25+ subsets of human CD4+ T cells.

Growing evidence suggests that the immunomodulatory heme oxygenase-1 (HO-1) may have an important role in regulating T-cell responses. In this study, we investigated whether CD4(+)CD25(-) and CD4(+)CD25(+) T cells of human CD4(+) subpopulation could differentially express HO-1. Our results obtained from qualitative reverse transcriptase-polymerase chain reaction and quantitative flow cytometry analyses revealed that the CD4(+)CD25(+) T cells constitutively express HO-1 and that T cell stimulation with plate-bound anti-CD3 in combination with soluble anti-CD28 not only induced HO-1 gene expression in the CD4(+)CD25(-) T cells but also up-regulated HO-1 gene expression in the CD4(+)CD25(+) T cells. Our further studies showed that CD28 signal alone was enough to induce HO-1 expression and CD3 signal, of which signal alone did not induce HO-1 expression, was required at least for full HO-1 expression in both CD25(-) and CD25(+) subsets of human CD4(+) T cells. In addition, transfection of human Jurkat T cells with HO-1 suppressed the cellular proliferation, and this effect was reversed by zinc protoporphyrin, a specific HO competitive inhibitor. Taken together, we have first reported that human CD4(+)CD25(+) regulatory T cells constitutively express HO-1 and that HO-1 inhibits Jurkat T cell proliferation.

CD28 Antigens↗

PubMed2003

Identification of novel polymorphisms in the Adam33 gene.

Adam33 is a member of a family of genes that encode membrane-anchored proteins with a disintegrin and a metalloprotease domain and that are primarily expressed in lung fibroblasts and bronchial smooth muscle. The human Adam33 gene is located on chromosome 20p13, a region that has been linked to asthma and bronchial hyperresponsiveness. Recently, the polymorphisms in Adam33 have been found to be associated with asthma. In this study, we performed polymorphism scanning of the entire genomic region, including the promoter region of Adam33, by direct sequencing. We identified 16 novel polymorphisms in the Adam33 gene. Among these novel polymorphisms, three polymorphisms (-2154G-->A, -753T-->A, and -330C-->T) were found to be in the promoter region and one polymorphism (13491 G-->A) was located in 3' untranslated region of the Adam33 gene.

3' Untranslated Regions↗

PubMed2003

Molecular variations in the promoter and coding regions of human Tim-1 gene and their association in Koreans with asthma.

The family of T-cell immunoglobulin domain and mucin domain (TIM) proteins is identified to be expressed on T cells. A member of Tim family, TIM-1, was considered as a membrane protein that is associated with the development of helper T cell (Th2) biased immune responses, and may be selectively expressed on Th2 cells. In the present study we performed single nucleotide polymorphism (SNP) scanning of the coding and promoter regions of human Tim-1 gene. We identified a total of ten SNPs including five novel SNPs (-1166C>G, -416G>C, -232A>G, 5365C>T, and 5529A>G) in the coding and promoter regions, one novel variation site (-2278_-2276dupATT) in the promoter region and three variations (5383_5397del, 5387_5389insAAC, and 5509_5511delCAA) in exon 4 of human Tim-1 gene. Our results suggest that the exon 4 variation site in human Tim-1 gene is associated with the susceptibility of allergic disease.

Asthma↗