Biomedical subjects

Tae-Hwan Kim

Publications and source records attributed to Tae-Hwan Kim.

41 records · Page 3Linked to original sources

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

Diagnostic evaluation of carbon tetrachloride-induced rat hepatic cirrhosis model.

BACKGROUND: To find a non-invasive method of diagnosing hepatic fibrosis and cirrhosis, we evaluated the relationship of the hepatic cirrhosis grade between histopathology and mean grey level (MGL) in B-mode ultrasonography in CCl4-induced liver cirrhosis. MATERIALS AND METHODS: Three groups of rats were treated with olive oil, CCl4, and CCl4 + silymarin. Rats were sacrificed at weeks 4, 8 and 12, after B-mode ultrasonography examination, and then analyzed histopathologically for fatty change and fibrosis. RESULTS: On the grade of fibrosis, the CCl4 group showed higher value at 8 and 12 weeks than the silymarin group. However, the fatty change was enhanced in the silymarin group, compared with the CCl4 group. The B-mode histogram values were the highest in the silymarin group, but the collagen rate was highest in the CCl4-treated group, at week 12. These results suggest that the B-mode histogram can be more affected by infiltration of lipid than by intact accumulation of collagen fibers. CONCLUSION: In the histogram of 8 and 12 weeks, there were significant differences between the CCl4-treated group and silymarin group in mean grey levels of B-mode ultrasonography. The histogram of B-mode mean grey level has a close correlation with fatty change and is useful for the diagnosis of liver fibrosis by histopathological analysis.

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PubMedDate not supplied

Expression of cytokeratins 8 and 18 on Mallory body and oval cell in rats during hepatic fibrosis.

BACKGROUND: The aim of this study was to determine the induction and distribution of Mallory body (MB) and oval cells in carbon-tetrachloride (CCl4)-induced rat liver fibrosis. MATERIALS AND METHODS: MBs and oval cells expressing cytokeratins (CKs) 8 and 18 were monitored by immuno-histochemistry and immunoblotting. RESULTS: MBs were mainly detected within hepatocytes near the fibrotic areas, and oval cells were located along or in the fibrotic areas. Both MBs and oval cells increased in size and number in the development of fibrosis. At cirrhotic liver, most of the oval cells were located in the fibrous septa and around newly formed bile ductules. Moreover, as hepatic injuries developed into fibrosis, a much more prominent single band of CK18 was detected. CONCLUSION: The occurrence and distribution of MB and oval cells in CCl4-induced rat liver fibrosis are reported. This represents the first CCl4 experimental in vivo model of MB induction, which will be useful for further investigations on the pathogenesis of MB.

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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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