Biomedical subjects

Jin Chung

Publications and source records attributed to Jin Chung.

7 recordsLinked to original sources

PubMed2006

Induction of RANTES and CCR5 through NF-kappaB activation via MAPK pathway in aged rat gingival tissues.

Chemokine and chemokine receptor expression in gingival tissues plays a central role in periodontal disease during aging. In the present study, we explored the modulation of chemokines and chemokine receptors expression in aging rat gingival tissues. In the 24-month-old (Old) rat gingival tissues, RANTES and CCR5 mRNA and protein levels were 2-4 fold increased over those of the 6-month-old (Young) rats. The Old rats had considerable enhancement of all three of the studied MAPK activities: extracellular signal regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAPK. These results suggest that age-related increases in RANTES and CCR5 expression are associated with increased IkappaBalpha, nuclear NF-kappaB, and MAPK activity in gingival tissues.

Aging↗

PubMed2006

Inhibitory effect of Weissella cibaria isolates on the production of volatile sulphur compounds.

AIMS: The objective of this study was to characterize the inhibitory effects of Weissella cibaria isolates on volatile sulphur compounds (VSC) production both in vitro and in vivo. MATERIAL AND METHODS: We isolated and identified three hydrogen peroxide-generating lactobacilli from children's saliva, and assessed their inhibitory effects on VSC production and Fusobacterium nucleatum proliferation. Clinical studies were conducted with 46 subjects in order to measure the VSC of their mouth air. RESULTS: These lactobacilli were identified as W. cibaria. These isolates inhibited the production of VSC by F. nucleatum (p<0.05). The concentration of F. nucleatum was decreased by 5-log cycles as a result of exposure to the W. cibaria strains (p<0.05), whereas the catalase-treated W. cibaria cultures exerted no evident inhibitory effects on F. nucleatum replication. In the clinical studies, gargling with one isolate resulted in a significant reduction in the levels of H2S and CH3SH by approximately 48.2% (p<0.01) and 59.4% (p<0.05), respectively. CONCLUSIONS: These results indicate that W. cibaria isolates possess the ability to inhibit VSC production under both in vitro and in vivo conditions, demonstrating that they bear the potential for development into novel probiotics for use in the oral cavity.

Adult↗

PubMed2005

Xylitol inhibits inflammatory cytokine expression induced by lipopolysaccharide from Porphyromonas gingivalis.

Porphyromonas gingivalis is one of the suspected periodontopathic bacteria. The lipopolysaccharide (LPS) of P. gingivalis is a key factor in the development of periodontitis. Inflammatory cytokines play important roles in the gingival tissue destruction that is a characteristic of periodontitis. Macrophages are prominent at chronic inflammatory sites and are considered to contribute to the pathogenesis of periodontitis. Xylitol stands out and is widely believed to possess anticaries properties. However, to date, little is known about the effect of xylitol on periodontitis. The aim of the present study was to determine tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) expression when RAW 264.7 cells were stimulated with P. gingivalis LPS (hereafter, LPS refers to P. gingivalis LPS unless stated otherwise) and the effect of xylitol on the LPS-induced TNF-alpha and IL-1beta expression. The kinetics of TNF-alpha and IL-1beta levels in culture supernatant after LPS treatment showed peak values at 1 h (TNF-alpha) and 2 to 4 h (IL-1beta), respectively. NF-kappaB, a transcription factor, was also activated by LPS treatment. These cytokine expressions and NF-kappaB activation were suppressed by pretreatment with pyrrolidine dithiocarbamate (an inhibitor of NF-kappaB). Pretreatment with xylitol inhibited LPS-induced TNF-alpha and IL-1beta gene expression and protein synthesis. LPS-induced mobilization of NF-kappaB was also inhibited by pretreatment with xylitol in a dose-dependent manner. Xylitol also showed inhibitory effect on the growth of P. gingivalis. Taken together, these findings suggest that xylitol may have good clinical effect not only for caries but also for periodontitis by its inhibitory effect on the LPS-induced inflammatory cytokine expression.

Animals↗

PubMed2003

Tip60 is a co-repressor for STAT3.

Tip60 (Tat-interactive protein, 60 kDa), a cellular protein with intrinsic histone acetyltransferase activity, is involved in DNA damage repair and apoptosis. Recent studies have suggested that Tip60 acts either as a co-activator or a co-repressor to modulate transcription. In this study, we demonstrate that Tip60 represses reporter gene expression when it is fused to the Gal4 DNA binding domain. We also show that Tip60 associates with histone deacetylase 7 (HDAC7) through its N-terminal zinc finger-containing region and that HDAC7 activity is required for the repressive effect of Tip60. Because endogenous Tip60 interacts with STAT3, we hypothesized that Tip60 might complex with STAT3 and HDAC7 and modulate STAT3-mediated trans-activation. Consistent with this hypothesis, the overexpression of Tip60 represses STAT3-driven reporter gene expression, which can be further potentiated by the co-transfection of HDAC7. Furthermore, interleukin-9-induced c-myc expression, which depends on STAT3 activity, is abrogated by exogenous expression of Tip60. This is the first demonstration of which Tip60 represses STAT3 activity in part through the recruitment of HDAC7.

Acetyltransferases↗

PubMed2003

Hydrogen peroxide-induced cell death in a human retinal pigment epithelial cell line, ARPE-19.

The loss of retinal pigment epithelium (RPE) with aging is related to age-related macular degeneration (AMD). This study was conducted to investigate the mechanism of hydrogen peroxide (H2O2) induced cell death in a human retinal pigment epithelial cell line, ARPE-19. Hydrogen peroxide was added at different concentrations to ARPE-19 cells and cultured. The cytotoxicity was assayed by mitochondrial function using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) testing. The patterns of cell damage were assessed using an acridine orange-ethidium bromide differential staining method, in situ end labeling (ISEL) assay and transmission electron microscopy (TEM). Catalase, a major antioxidant, was used to prevent cell death. The cleavage of procaspase 3 and poly (ADP-ribose) polymerase (PARP) was determined by western blot analysis. Hydrogen peroxide significantly induced cell death in ARPE-19 cells, whereas pretreatment of the cells with catalase prevented cell death. Application of the ISEL assay and acridine orange/ethidium bromide staining demonstrated that the H2O2-induced cell death occurred by an apoptotic mechanism at lower concentrations of H2O2 (400, 500, 600 microM), whereas higher concentrations of H2O2 induced necrosis rather than apoptosis. Caspase 3 was associated with the apoptotic pathway in human RPE cell death. Western blot analysis confirmed caspase 3 activation and cleavage of substrate proteins in ARPE-19 cells treated with an H2O2 concentration of 600 microM. These results indicate that treatment with H2O2 induces apoptotic and necrotic cell death in ARPE-19, and that caspase 3 is associated with apoptotic cell death. Therefore, H2O2 may induce the destruction of RPE cells in AMD by the combined effects of apoptosis and necrosis.

Apoptosis↗

PubMed2002

Specificity of interleukin-2 receptor gamma chain superfamily cytokines is mediated by insulin receptor substrate-dependent pathway.

Interleukins 9 (IL-9) and 4 are cytokines within the IL-2 receptor gamma chain (IL-2R gamma) superfamily that possess similar and unique biological functions. The signaling mechanisms, which may determine cytokine specificity and redundancy, are not well understood. IRS proteins are tyrosine-phosphorylated following IL-9 and IL-4 stimulation, a process in part mediated by JAK tyrosine kinases (Yin, T. G., Keller, S. R., Quelle, F. W., Witthuhn, B. A., Tsang, M. L., Lienhard, G. E., Ihle, J. N., and Yang, Y. C. (1995) J. Biol. Chem. 270, 20497--20502). In the present study, we used 32D cells stably transfected with insulin receptor (32D(IR)), which do not express any IRS proteins, as a model system to study the requirement of different structural domains of IRS proteins in IL-9- and IL-4-mediated functions. Overexpression of IRS-1 and IRS-2, but not IRS-4, induced proliferation of 32D(IR) cells in response to IL-9. The pleckstrin homology (PH) domain of IRS proteins is required for IRS-mediated proliferation stimulated by IL-9. The phosphotyrosine binding and Shc and IRS-1 NPXY binding domains are interchangeable for IRS to transduce the proliferative effect of IL-4. Therefore, the PH domain plays different roles in coupling IRS proteins to activated IL-9 and IL-4 receptors. The role of IRS proteins in determining cytokine specificity was corroborated by their ability to interact with different downstream signaling molecules. Although phosphatidylinositol 3' -kinase (PI3K) and Grb-2 interact with tyrosine-phosphorylated IRS proteins, Shp-2 only binds to IRS proteins following IL-4, but not IL-9, stimulation. Although PI3K activity is necessary for the IRS-1/2-mediated proliferative effect of IL-9 and IL-4, Akt activation is only required for cell proliferation induced by IL-4, but not IL-9. These data suggest that IRS-dependent signaling pathways work by recruiting different signaling molecules to determine specificity of IL-2R gamma superfamily cytokines.

Adaptor Proteins, Signal Transducing↗

PubMed2002

Effect of cataract surgery on the progression of diabetic retinopathy.

PURPOSE: To study the effect of cataract surgery and other factors on the progression of diabetic retinopathy using the nonoperated contralateral eye as a control. SETTING: Department of Ophthalmology, Catholic University Medical College, Uijongbu St. Mary's Hospital, Seoul, Korea. METHODS: Monocular cataract surgery was performed in 75 patients who had the same degree of retinopathy or no retinopathy in both eyes preoperatively. Patients were assigned to 1 of 2 groups as follows: Group A, progression of retinopathy in the operated eye caused by cataract surgery; Group B, no progression of retinopathy bilaterally, comparable level of progression in both eyes, or more progression of retinopathy in the nonoperated eye than in the operated eye. The differences between the 2 groups in age, duration of and treatment methods for diabetes, renal function, and presence of preoperative macular edema were compared. The 1-year follow-up included evaluation of the progression of retinopathy. RESULTS: Surgery caused the retinopathy to progress in 23 patients (30.6%, Group A); 52 patients (69.4%, Group B) had no progression of retinopathy or a comparable level of retinopathy postoperatively. The operated eye had more progression of retinopathy than the nonoperated contralateral eye (P <.05). There was no significant difference between the 2 groups in age, diabetes duration, surgical method, or hypertension. Preoperative macular edema and poor renal function significantly affected the progression of diabetic retinopathy after cataract surgery (P <.05). CONCLUSIONS: Diabetic retinopathy progressed after cataract surgery. The presence of preoperative macular edema and poor renal function increased the progression of retinopathy postoperatively.

Capsulorhexis↗