Biomedical subjects

Seongyong Kim

Publications and source records attributed to Seongyong Kim.

4 recordsLinked to original sources

PubMed2004

Exploration of replicative senescence-associated genes in human dermal fibroblasts by cDNA microarray technology.

The aging process is known to be regulated by specific genes in various organisms, including yeast, the nematode C. elegans, fruitflies and mice. To explore the novel genes involved in aging process, we applied cDNA microarray technology to a replicative senescence model of human dermal fibroblasts (HDF). Eighty-four genes, including inflammatory genes, cell cycle regulatory genes, cytoskeletal genes, and metabolic genes were found to show more than two fold expressional differences in young and old fibroblasts. Furthermore, 31 genes were confirmed to be up- or down-regulated during replicative senescence by semi-quantitative RT-PCR. The overexpressions of several genes including CD36, putative lymphocyte G0/G1 switch gene (G0S2), tumor protein D52-like 1 (TPD52L1), chemokine (C-X-C motif) ligand 6, myxovirus resistant gene 1 (MX1), and the down-regulation of the immunoglobulin superfamily containing leucine-rich repeat (ISLR), neurotrimin, insulin-like growth factor 2 associated protein (IGF2A), and apoptosis-related RNA binding protein (NAPOR3) were newly identified. These results suggest that fibroblasts show the deregulation of various cellular processes, such as inflammatory response, mitosis, cell adhesion, transport, signal transduction, and metabolism during replicative senescence.

Cell Division↗

PubMed2003

Identification of amyloid beta-peptide responsive genes by cDNA microarray technology: involvement of RTP801 in amyloid beta-peptide toxicity.

Amyloid beta-peptide (Abeta), a causative molecule in the pathogenesis of Alzheimer's disease and the main component of senile plaques, is known to be neurotoxic in vitro and in vivo. The mechanisms involved in this Ab-mediated neurotoxicity are not fully understood, although there is evidence to suggest the involvement of oxidative stress, alterations in calcium homeostasis, and/or of CDK activators. Many studies have suggested that Ab may exert its toxic effect via the activation of transcription factors. Therefore, we investigated Ab- responsive genes in human neuroblastoma CHP134 cells using 3.1K human DNA microarrays. Among the several genes overexpressed or repressed by Ab, RTP801, Hi95/sestrin 2, and stanniocalcin 2 were confirmed to be Ab-mediated overexpression in the cells by semiquantitative RT-PCR. Transient expression of the sense RTP801 gene in CHP134 cells increased sensitivity to Abeta cytotoxicity and the expression of the antisense RTP801 gene protected the cells from the Abeta toxicity. These results suggest that RTP801 might play important roles in Abeta toxicity and the pathogenesis of Alzheimer's disease.

Alzheimer Disease↗

PubMed2003

Involvements of mitochondrial thioredoxin reductase (TrxR2) in cell proliferation.

Mammalian cells contain two forms of thioredoxin reductase (TrxR), cytosolic TrxR1 and mitochondrial TrxR2. To investigate the biological roles of TrxR2, we generated stable HeLa cell lines expressing a dominant negative form of TrxR2 (TrxR2DN) under the control of the tetracycline-off system. We observed that TrxR2DN-induced cells, following stimulation with EGF, produced more hydrogen peroxide than uninduced cells. The extent of protein tyrosine phosphorylation of many proteins including ERK was higher in TrxR2DN-induced cells than in uninduced cells when stimulated with fetal bovine serum or EGF. Induction of TrxR2DN also resulted in the increased rate of progression of G1 to S phase in cell cycle and cell proliferation and affected the expression of many proteins involved in cell cycle. These results suggest that TrxR2 participates in the regulation of protein tyrosine phosphorylation and cell growth as a component of the mitochondria specific H2O2-eliminating system that includes peroxiredoxin III and thioredoxin 2.

Cell Cycle↗

PubMedDate not supplied

Overexpression of mitochondrial thioredoxin reductase and peroxiredoxin III in hepatocellular carcinomas.

Thioredoxin reductase 2 (TrxR2), thioredoxin II (Trx II) and peroxiredoxin III (Prx III) are specifically localized in mitochondria and believed to play important roles in the regulation of cellular redox status by serving as a primary line of defense against H2O2 produced during respiration. Substantial evidence indicates that the alteration of cellular redox status is a critical factor involved in cell growth and death and results in tumorigenesis. We therefore investigated the expression of TrxR2 and Prx III in 58 paraffin-embedded hepatocellular carcinoma tissues by immunohistochemistry. The labeling indices of TrxR2 and Prx III were significantly higher in tumor tissues than in the corresponding adjacent normal tissues. In 39 (67.2%) out of 58 samples, the levels of TrxR2 expression were higher in tumor tissues than in corresponding adjacent normal tissues, while 11 samples (19.0%) showed lower expression in tumor tissues. Prx III expression was increased in tumor tissues of 23 samples (39.7%) compared to adjacent normal tissues and were decreased in 18 samples (31.0%). These results suggest that alterations in cellular redox status by enhanced expression of TrxR2 and/or Prx III might be associated with the formation and development of hepatocellular carcinomas.

Adult↗