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Ja-Young Kim

Publications and source records attributed to Ja-Young Kim.

11 recordsLinked to original sources
PubMed2006

Keystone meeting summary: 'Adipogenesis, obesity, and inflammation' and 'Diabetes mellitus and the control of cellular energy metabolism, ' January 21-26, 2006, Vancouver, Canada.

The dysregulation of specific cellular functions in adipocytes, muscle cells, beta cells, and the liver leads to changes in systemic metabolic processes and ultimately to the pathophysiological manifestations that cause type 2 diabetes. The underlying cellular mechanisms are complex. The two meetings summarized here aimed to highlight the recent advances in our understanding of the molecular basis of feeding and nutrient storage and on the molecular consequences of obesity in terms of promoting risk for type 2 diabetes and cardiovascular disease.

Adipogenesis↗
PubMed2006

Role of transcription factor NFAT in glucose and insulin homeostasis.

Compromised immunoregulation contributes to obesity and complications in metabolic pathogenesis. Here, we demonstrate that the nuclear factor of activated T cell (NFAT) group of transcription factors contributes to glucose and insulin homeostasis. Expression of two members of the NFAT family (NFATc2 and NFATc4) is induced upon adipogenesis and in obese mice. Mice with the Nfatc2-/- Nfatc4-/- compound disruption exhibit defects in fat accumulation and are lean. Nfatc2-/- Nfatc4-/- mice are also protected from diet-induced obesity. Ablation of NFATc2 and NFATc4 increases insulin sensitivity, in part, by sustained activation of the insulin signaling pathway. Nfatc2-/- Nfatc4-/- mice also exhibit an altered adipokine profile, with reduced resistin and leptin levels. Mechanistically, NFAT is recruited to the transcription loci and regulates resistin gene expression upon insulin stimulation. Together, these results establish a role for NFAT in glucose/insulin homeostasis and expand the repertoire of NFAT function to metabolic pathogenesis and adipokine gene transcription.

AMP-Activated Protein Kinases↗
PubMed2005

Prevalence of decreased susceptibility to carbapenems among Serratia marcescens, Enterobacter cloacae, and Citrobacter freundii and investigation of carbapenemases.

Between March and July 2002, total of 612 clinical isolates of Serratia marcescens, Enterobacter cloacae, and Citrobacter freundii (201 S. marcescens, 228 E. cloacae, and 183 C. freundii) were collected from 13 clinical laboratories in a nationwide distribution. Imipenem and meropenem minimum inhibitory concentrations (MICs) were determined using the agar dilution method according to the National Committee for Clinical Laboratory Standards guidelines. For the isolates with a decreased susceptibility to carbapenems (MICs of >or=2 microg/mL), isoelectric focusing, polymerase chain reaction (PCR) amplification of the carbapenemase genes (bla(IMP-1), bla(VIM-2), bla(SME-1), bla(OXA-23), bla(OXA-25), bla(KPC-1)), and sequencing were performed. The prevalence of S. marcescens, E. cloacae, and C. freundii with a decreased susceptibility to imipenem was 17.9% (36/201), 0.4% (1/228), and 0.5% (1/183), respectively, and to meropenem, it was 11.4% (23/201), 0% (0/228), and 0.5% (1/183), respectively. The bla(VIM-2) was the only carbapenemase detected, and was found in 0.5% (1/201) of S. marcescens and 0.5% (1/183) of C. freundii isolate.

Anti-Bacterial Agents↗
PubMed2004

Nosocomial outbreak by Proteus mirabilis producing extended-spectrum beta-lactamase VEB-1 in a Korean university hospital.

OBJECTIVES: To examine the molecular mechanisms involved in the beta-lactam resistance of multidrug-resistant Proteus mirabilis isolates that showed an unusual synergy between imipenem and ceftazidime in a Korean hospital. METHODS: Over an 11 month period, a total of 12 P. mirabilis isolates showing resistance to ampicillin, gentamicin, ceftazidime, cefotaxime, cefuroxime, cefalothin, cefepime, piperacillin, trimethoprim/sulfamethoxazole and ciprofloxacin, were recovered from the sputum and urine specimens of nine patients who were hospitalized in the neurosurgery ward. The extended-spectrum beta-lactamases were screened with a double disc synergy test using ceftazidime, cefotaxime, aztreonam, cefepime and clavulanate. The ESBL types were determined by PCR using specific primers for bla(TEM-1), bla(SHV-1), bla(CTX-M-1), bla(CTX-M-2), bla(CTX-M-8), bla(CTX-M-9), bla(PER-1), bla(GES-1), bla(VEB-1), bla(OXA-10) and bla(OXA-13) followed by sequencing. All the isolates underwent molecular typing by PFGE. The transferability was examined by conjugation. RESULTS AND CONCLUSIONS: All the isolates showed a marked synergy between the extended-spectrum cephalosporins and clavulanate together with an unusual synergy between cefoxitin and the cephalosporins (cefalothin, cefuroxime, ceftazidime, cefotaxime) and between imipenem, and ceftazidime and cefotaxime. Isoelectric focusing of the crude bacterial extracts showed a beta-lactamase band with a pI value of 5.4, which was inhibited by clavulanate. PCR and sequencing identified the gene to be bla(VEB-1). In addition, the aadB gene was detected, conferring aminoglycoside resistance. The resistance was not transferred by conjugation. The outbreak was of a clonal origin as shown by PFGE demonstrating an identical banding pattern. This is the first report of VEB-1-producing Enterobacteriaceae in Korea.

Anti-Bacterial Agents↗
PubMed2004

Resistance of rho(0) cells against apoptosis.

Mitochondrion is one of the master players in both apoptosis and necrosis. However, most previous articles report that mitochondrial DNA-depleted cells without oxidative phosphorylation underwent apoptosis by several apoptotic effectors as efficiently as their parental cells, suggesting that intact mitochondrial function is dispensable for the progression of apoptosis. We studied the role of mitochondrial function in several apoptosis models. TRAIL, a recently identified member of the TNF family with cytotoxicity on a wide variety of transformed cells, killed SK-Hep1 cells with characteristic features of apoptosis such as DNA fragmentation, sub-G1 ploidy peak, and cytochrome c translocation. In contrast with parental cells, mitochondrial DNA-deficient SK-Hep1 rho(0) cells were resistant to TRAIL-induced apoptosis. Dissipation of mitochondrial potential or cytochrome c translocation did not occur in rho(0) cells after TRAIL treatment. Bax translocation also was absent in rho(0) cells, accounting for the failure of cytochrome c release in rho(0) cells. SK-Hep1 rho(0) cells were resistant to other death effectors such as staurosporine. Our results indicate that apoptosis of SK-Hep1 hepatoma cells is dependent on intact mitochondrial function. Because aged cells or tumor cells have frequent mutations or deletions of mitochondrial DNA, they might acquire the ability to evade apoptosis or tumor surveillance imposed by TRAIL or other death effectors in vivo, accounting for the selection advantage of cancer cells and frequent development of cancer in aged individuals.

Antineoplastic Agents↗
PubMed2004

Case report: Bacteremia due to Salmonella enterica Serotype Montevideo producing plasmid-mediated AmpC beta-lactamase (DHA-1).

A Salmonella enterica Serotype Montevideo is described that harbors DHA-1, a plasmid-mediated AmpC beta-lactamase. The organism was isolated from blood and stool specimens of a 3-yr-old girl. The isolate was multi-drug resistant, including cefoxitin, gentamicin, piperacillin, cefuroxime, ceftazidime, and cefotaxime, and an antagonism was observed between cefoxitin and oxyiminocephalosporins. The resistance to ceftazidime and cefotaxime was transferred by conjugation to the recipient E. coli J53. To our knowledge, this is the first description of Salmonella enterica Serotype Montevideo harboring DHA-1.

Bacteremia↗
PubMed2004

Adiponectin, an adipocyte-derived hepatic insulin sensitizer regulation during development.

A large body of clinical data, supported by genetic and pharmacological evidence, has demonstrated potent insulin-sensitizing effects of the adipocyte-derived secretory factor adiponectin. In adults, plasma adiponectin is generally negatively correlated with BMI and positively correlated with systemic insulin sensitivity. Only a limited number of studies have been performed in newborns, children and adolescents. Here we summarize the results from these recent findings in younger cohorts and discuss these results in context of the much vaster literature on adiponectin levels in lean, obese and diabetic adults.

Adiponectin↗
PubMed2003

Resistance of mitochondrial DNA-depleted cells against cell death: role of mitochondrial superoxide dismutase.

We have shown that mitochondrial DNA-depleted (rho(0)) SK-Hep1 hepatoma cells are resistant to apoptosis, contrary to previous papers reporting normal apoptotic susceptibility of rho(0) cells. We studied the changes of gene expression in SK-Hep1 rho(0) cells. DNA chip analysis showed that MnSOD expression was profoundly increased in rho(0) cells. O(2)(.) contents increased during rho(0) cell derivation but became normalized after establishment of rho(0) phenotypes, suggesting that MnSOD induction is an adaptive process to increased O(2)(.). rho(0) cells were resistant to menadione, paraquat, or doxorubicin, and O(2)(.) contents after treatment with them were lower in rho(0) cells compared with parental cells because of MnSOD overexpression. Expression levels and activity of glutathione peroxidases were also increased in rho(0) cells, rendering them resistant to exogenous H(2)O(2). rho(0) cells were resistant to p53, and intracellular ROS contents after p53 expression were lower compared with parental cells. Other types of rho(0) cells also showed increased MnSOD expression and resistance against ROS. Heme oxygenase-1 expression was increased in rho(0) cells, and a heme oxygenase-1 inhibitor decreased the induction of MnSOD in rho(0) cells and their resistance against ROS donors. These results indicate that rho(0) cells are resistant to cell death contrary to previous reports and suggest that an adaptive increase in the expression of antioxidant enzymes renders cancer cells or aged cells with frequent mitochondrial DNA mutations to resist against oxidative stress, host anti-cancer surveillance, or chemotherapeutic agents, conferring survival advantage on them.

Animals↗
PubMed2002

Resistance of mitochondrial DNA-deficient cells to TRAIL: role of Bax in TRAIL-induced apoptosis.

Mitochondrion is one of the master players in both apoptosis and necrosis. We studied the role of mitochondrial function in TRAIL-induced apoptosis. TRAIL killed SK-Hep1 cells with characteristic features of apoptosis such as DNA fragmentation, sub-G1 ploidy peak and cytochrome c translocation. In contrast, mitochondrial DNA-deficient SK-Hep1 rho(0) cells were resistant to TRAIL. Dissipation of mitochondrial potential or cytochrome c translocation did not occur in rho(0) cells after TRAIL treatment. TRAIL induced translocation of Bax subsequent to the cleavage of Bid in parental cells. However, Bax translocation was absent in rho(0) cells, accounting for the failure of cytochrome c release in rho(0) cells. Forced expression of Bax induced caspase-3 activity in rho(0) cells. Incubation of rho(0) cells with ADP+Pi to increase intracellular ATP restored sensitivity to TRAIL. Despite different sensitivity to TRAIL, parental cells and rho(0) cells did not show significant difference in susceptibility to agonistic anti-Fas antibody, TNF-alpha or staurosporine. Our results indicate that TRAIL-induced apoptosis is dependent on intact mitochondrial function and susceptibility of mitochondrial DNA-deficient cells to apoptosis depends on the type of apoptotic stimuli. Tumor cells with mitochondrial mutations or dysfunction might have the ability to evade tumor surveillance imposed by TRAIL in vivo.

Adenosine Triphosphate↗
PubMed2002

Involvement of p38 mitogen-activated protein kinase in the cell growth inhibition by sodium arsenite.

It is well-known that p38 mitogen-activated protein kinase (p38MAPK) participates in cellular responses to mitogenic stimuli, environmental and genotoxic stresses, and apoptotic agents. Although there are several reports on p38MAPK in relation to cell growth and apoptosis, the exact mechanism of p38MAPK-mediated cell growth regulation remains obscure. Here, we examined possible roles of p38MAPK in the sodium arsenite-induced cell growth inhibition in NIH3T3 cells. Sodium arsenite induced transient cell growth delay with marked activation of p38MAPK. In addition, arsenite induced CDK inhibitor p21(CIP1/WAF1) and enhanced its binding to the CDK2, which resulted in inhibition of CDK2 activity. The levels of cyclin D1 expression and the CDK4 kinase activity were also significantly reduced. pRB was hypophosphorylated by sodium arsenite. SB203580, a specific inhibitor of p38MAPK, blocked arsenite-induced growth inhibition as well as the arsenite-induced p21(CIP1/WAF1) expression. Expression of dominant negative p38MAPK also blocked arsenite-induced p21(CIP1/WAF1) expression. Inhibited-CDK2 activity was also completely reversed by SB203580 or expression of dominant negative p38MAPK, while the decreased-cyclin D1 protein by the compound was not restored. These data demonstrate a possible link between the activation of p38MAPK and induction of p21(CIP1/WAF1), suggesting that the activation of p38MAPK is, at least in part, related to the cell growth inhibition by sodium arsenite.

3T3 Cells↗