Biomedical subjects

Won-Kee Yoon

Publications and source records attributed to Won-Kee Yoon.

5 recordsLinked to original sources

PubMed2006

Reactive oxygen species augment B-cell-activating factor expression.

B-cell-activating factor (BAFF) plays a role in mature B-cell generation and maintenance. Lipopolysaccharide (LPS) activates toll-like receptor 4 (TLR4)-dependent signal transduction and induces ROS production. Here, we investigated BAFF production regulated by reactive oxygen species (ROS). BAFF expression was augmented by LPS stimulation and by serum deprivation that induced ROS production. BAFF expression was inhibited by treatment with various antioxidants including N-acetyl-L-cysteine (NAC). We also investigated BAFF expression in vivo using peroxiredoxin II (PrxII)-deficient mouse spleen cells. PrxII is a member of the antioxidant enzyme family that protects cells from oxidative damage. Constitutive production of endogenous ROS was detected in spleen cells lacking PrxII. Serum BAFF protein level and BAFF transcript expression in splenocytes were significantly higher in PrxII(-/-) mice than wildtype mice. A higher BAFF level is consistent with the higher total number of splenocytes and B220(+)cells. Results were supported by NF-kappaB activation as judged by reduced IkappaBalpha degradation and increased nuclear translocation of p65/RelA with LPS stimulation, serum deprivation, and PrxII deletion. Data suggest that TLR4-mediated BAFF expression was increased by ROS and it was inhibited by PrxII controlling ROS production.

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PubMed2005

Somatostatin down-regulates LFA-1 activation by modulating Rap1 expression in CD4+ and CD8+ T cells.

Leukocyte function-associated antigen-1 (LFA-1) is one of the integrins that are expressed on the leukocytes, and has been shown to play an important role in leukocyte trafficking. The adhesive activity of LFA-1 is governed partially by the Rap1. This study examined that the relationship between LFA-1 and Rap1 mRNA expressions by anti-CD3 and anti-CD3+SOM treatment in the CD4+ and CD8+ T cells. The LFA-1 mRNA expression levels following the anti-CD3 and anti-CD3+SOM treatment for 30 min was greater on the CD8+ T cells, and the LFA-1 expression of the CD8+ T cells with anti-CD+SOM treatment was affected more severely than that of the CD4+ T cells. The Rap1 mRNA expression patterns following anti-CD3 and anti-CD3+SOM stimulation in the CD4+ and CD8+ T cells were similar to the LFA-1 expression patterns, and the expression level following anti-CD3+SOM treatment was suppressed more significantly in the CD8+ T cells. These results suggest that the difference in the Rap1 expression level after stimulation might explain the differences in the LFA-1 expression level on the T cell subsets, and that the down-regulation of Rap1 expression following SOM treatment is closely related to the diminished LFA-1 expression.

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PubMedDate not supplied

Somatostatin controls LFA-1 gene expression by altering neuraminidase expression in spleen cells.

This study investigated whether neuraminidase (Neu) affects LFA-1 mRNA expression in spleen cells and whether somatostatin (SOM) and substance P (SP) treatment induce changes in the Neu mRNA expression level in spleen cells. Neu treatments down-regulated the LFA-1 mRNA levels after culturing for 2 h. SOM increased the Neu mRNA level slightly after 24-h culture and strongly after 48-h culture. These results suggest that prolonged exposure to SOM may regulate the Neu activation pathway, which in turn impairs the regulation of LFA-1 expression.

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PubMedDate not supplied

2,3,7,8-Tetrachlorodibenzo-p-dioxin activates ERK and p38 mitogen-activated protein kinases in RAW 264.7 cells.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widespread environmental contaminant, exposure to it eliciting a broad spectrum of deleterious pathophysiological effects. Since mitogen-activated protein kinase (MAPK) pathways appear to play an important role in both cell survival and the apoptotic process, we assessed the effects of TCDD on the activation of extracellular signal-regulated kinase (ERK), Jun-N-terminal kinase (JNK), p38 MAPKs and caspase-3 in RAW 264.7 cells. TCDD treatment induced a transient upshift in ERK activity, followed by a decline, but a concomitant dramatic activation of p38. However, TCDD did not cause any apparent change in the activity of JNK, though it induced an up-regulation in caspase-3 activity. These results demonstrate that the equilibrium between the ERK and p38 pathways is critical to the fate of the cells, and that the activation of p38, upstream of caspase, plays an important role in the apoptotic process. The data obtained in this study also suggests that TCDD activates the MAPK pathway via an arylhydrocarbon receptor (AhR)-independent mechanism in RAW 264.7 murine macrophages.

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PubMedDate not supplied

Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on leukocyte function-associated antigen-1 mediated splenocyte adhesion.

2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a widespread environmental contaminant that induces various types of immunotoxicity. One effect of exposure to this contaminant is alteration in cell adhesiveness. Leukocyte function-associated antigen-1 (LFA-1) plays an important role not only in T-cell recruitment into sites of inflammation and lymphoid tissues, but also in T-cell activation and in the development of specific immune responses. We, therefore, examined whether the alteration in cell adhesiveness is associated with the modulation of LFA-1 expression and its second messengers following exposure to TCDD. In vitro, 10 nM TCDD exposure suppressed splenocyte adhesion. In addition, the adhesiveness was reduced after in vivo exposure to TCDD (15 microg/kg) for six weeks with a one week interval and after additional in vitro stimulation with anti-CD3. The inhibition of adherence after TCDD exposure was related to a decreased expression of LFA-I, and expression patterns of Rap1 following TCDD exposure correlated with those of LFA-1 expression. However, TCDD did not selectively alter LFA-1 or Rapl expression in T-cell subsets. TCDD caused apparent changes in PI 3-kinase expression levels and the expression patterns of H-Ras correlated with those of PI 3-kinase expression. These data suggest that TCDD exposure down-regulates the conformation and ligand binding affinity of LFA-1 by Rapl and PI 3-kinase signaling pathways with the decreased expression of LFA-1, and consequently leads to a decrease in the LFA-1-mediated adhesion.

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