Biomedical subjects

Tae Soo Kim

Publications and source records attributed to Tae Soo Kim.

24 records · Page 2Linked to original sources

PubMed2003

A novel model for rapid induction of apoptosis in spiral ganglions of mice.

OBJECTIVES/HYPOTHESIS: The survival of the spiral ganglion (SG) is a critical issue in preservation of hearing. Research on topics related to this issue requires a mouse experimental model because such a model has advantages including use of genetic information and knockout or "knockin" mice. Thus, the aim of the study was to establish a mouse model for induction of apoptosis of SG neurons with a definite time course. STUDY DESIGN: Laboratory study using experimental animals. METHODS: C57BL/6 mice were used as experimental animals and were subjected to direct application of cisplatin into the inner ear. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay and immunostaining for Neurofilament 200-kD (NF) and peripherin were used for analysis of SG degeneration. In addition, generation of peroxynitrite in affected spiral ganglions was examined by immunostaining for nitrotyrosine. Cellular location of activated caspase-9 and cytochrome-c in dying SG neurons were examined for analysis of cell death pathway. RESULTS: The TUNEL assay and immunohistochemical analysis for NF and peripherin indicated that type I neurons in spiral ganglions were deleted through the apoptotic pathway over time. Spiral ganglion neurons treated with cisplatin exhibited expression of nitrotyrosine, indicating induction of peroxynitrite by cisplatin. In dying SG neurons, expression of activated caspase-9 and translocation of cytochrome-c from mitochondria to cytoplasm were observed, indicating the mitochondrial pathway of apoptosis. CONCLUSION: The predictable fashion of induction of apoptosis in SG neurons over a well-defined time course in the model in the study will aid studies of the molecular mechanism of cell death and elucidation of a strategy for prevention of SG degeneration.

Animals↗

PubMed2002

Alteration in expression of p27 in auditory epithelia and neurons of mice during degeneration.

The aim of this study was to examine roles of p27, a cyclin-dependent kinase inhibitor, in cochleae of adult mice. Expression of p27 was found in cochlear supporting cells and spiral ganglion neurons of normal mice. Cisplatin treatment caused progressive degeneration of cochlear supporting cells and spiral ganglion neurons, and numbers of p27-positive cells in these cells decreased. This indicates a close relationship between p27 and cell death in cochleae. However, the relationships between decrease in number of p27-positive cells and that of survival cells differed according to type of cell. For Deiters' cells, there was apparent decrease in number of p27-positive cells, although no decrease in cell numbers. The present findings indicate that p27 plays roles in degeneration of cochleae according to cell type.

Animals↗

PubMed2002

Alteration of E-cadherin and beta-catenin in mouse vestibular epithelia during induction of apoptosis.

The aim of this study was to examine if adhesion molecules had relation with degeneration and regeneration processes of mammalian vestibular epithelia. The distribution of E-cadherin and beta-catenin was immunohistochemically examined in normal and aminoglycoside-treated utricles of mice. E-cadherin and beta-catenin linearly expressed between epithelial cells in normal specimens. Aminoglycoside injury resulted in temporal alteration in distribution of these molecules with induction of apoptosis in hair cells. Degradation of both molecules was widely observed in vestibular epithelia, while some supporting cells exhibited accumulation of beta-catenin. After completion of induction of apoptosis, expression of these adhesion molecules was normal in distribution. These findings suggest that the E-cadherin-beta-catenin complex plays roles in degeneration and subsequent repair processes in vestibular epithelia affected by aminoglycosides.

Aminoglycosides↗

PubMed2002

Selenoprotein W is a glutathione-dependent antioxidant in vivo.

The function of selenoprotein W (Se-W) was investigated by cloning the corresponding cDNA from mouse brain and expressing it in CHO cells and H1299 human lung cancer cells. Overexpression of Se-W markedly reduced the sensitivity of both cell lines to H2O2 cytotoxicity. The intracellular peroxide concentration of the transfected cells was lower than that of the parental cells in the absence or presence of extracellular H2O2. The resistance to oxidative stress conferred by Se-W was dependent on glutathione. Expression of Se-W mutants in which selenocysteine-13 or cysteine-37 was replaced by serine did not confer resistance to H2O2, implicating these residues in the antioxidant activity of Se-W in vivo.

Animals↗

PubMed2002

Protection of mice from allergen-induced asthma by selenite: prevention of eosinophil infiltration by inhibition of NF-kappa B activation.

The potential anti-inflammatory effect of sodium selenite in a mouse model of asthma was investigated. Selenite was injected into the peritoneum of allergen (ovalbumin)-sensitized mice before allergen challenge. Ovalbumin challenge resulted in activation of the transcription factor NF-kappaB and an increase in the expression of cell adhesion molecules (intercellular adhesion molecule 1, vascular cell adhesion molecule 1, and E-selectin, which are encoded by NF-kappaB-dependent genes) in lung tissue as well as in the recruitment of eosinophils to lung airways. These effects of ovalbumin challenge were all inhibited by pretreatment of mice with selenite. Selenite administration also increased the activity of selenium-dependent glutathione peroxidase in lung tissue. Furthermore, supplementation of A549 human airway epithelial cell cultures with selenite increased glutathione peroxidase activity as well as inhibited both the generation of hydrogen peroxide and the activation of NF-kappaB induced by tumor necrosis factor alpha in these cells. Selenite also reversed in vitro the activation of NF-kappaB induced by this cytokine in intact A549 cells. These results suggest that selenite regulates the activity of NF-kappaB by increasing the activity of glutathione peroxidase, thereby removing potential activators of NF-kappaB, and possibly also by direct oxidation of critical sulfhydryl groups of this transcription factor. These effects of selenite likely underlie its anti-inflammatory action in asthma.

Allergens↗

PubMed2002

Germination inhibitory constituents from Erigeron annuus.

(5-Butyl-3-oxo-2,3-dihydrofuran-2-yl)-acetic acid was isolated from the flowers of Erigeron annuus as one of four germination inhibitory constituents. Its structure was determined by analysis of MS and NMR spectroscopic data. Three known compounds, 3-hydroxy-pyran-4-one, 4-hydroxycinnamic acid, and 3,4-dihydroxycinnamic acid methyl ester were also identified as active constituents. These compounds showed 50% inhibitory effects (IC(50)) on the germination of lettuce seed at concentrations of 2.13+/-0.03, 12.85+/-0.56, 4.97+/-0.24, and 4.87+/-0.25 mM, respectively. 4-Hydroxybenzoic acid was used as a positive control, displaying an IC(50) value of 4.02+/-0.39 mM.

Asteraceae↗