Kwon Jeong

Kyung Hee University, Sŏul, Seoul, South Korea

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Publications (8)21.36 Total impact

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    ABSTRACT: Treatment with thapsigargin, a stimulator of p53 expression and an inducer of ER stress, decreased Pin1 expression in HCT116 cells.•Functional p53 response elements (p53REs) was identified in the Pin1 promoter.•Overexpression of p53 significantly decreased Pin1 expression in HCT116 cells while abolition of p53 gene expression induced Pin1 expression.•Pin1 expression was significantly increased by treatment with the p53 inhibitor pifithrin-α or down-regulation of p53 expression.•We demonstrated that ER stress decreases Pin1 expression through p53 activation.
    Biochemical and Biophysical Research Communications 10/2014; · 2.28 Impact Factor
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    ABSTRACT: Apelin, which is an endogenous ligand for the orphan G-protein-coupled receptor APJ, was reported to be up-regulated by hypoxia-inducible factor 1-α (HIF1-α) in hypoxia- and insulin-treated cell systems. However, a negative transcriptional regulator of apelin has not yet been identified. In this study, we showed that apelin is down-regulated by ATF4 via the pro-apoptotic p38 MAPK pathway under endoplasmic reticulum (ER) stress. First, we analyzed the human apelin promoter to characterize the effects of ER stress on apelin expression in hepatocytes. Treatment with thapsigargin, an inducer of ER stress, and over-expression of ATF4 decreased apelin expression in hepatocytes. This work identified an ATF4-responsive region within the apelin promoter. Interestingly, ATF4-mediated repression of apelin was dependent upon the N-terminal domain of ATF4. C/EBP-β knockdown experiments suggest that C/EBP-β, which acts as an ATF4 binding partner, is critical for the ER stress-induced down-regulation of apelin. We also demonstrated that ATF4 regulates apelin gene expression via p38 pathways. Ectopic expression of constitutively active MKK6, an upstream kinase of p38, suggested that activation of the p38 pathway is sufficient to induce ATF4-mediated repression of apelin. Moreover, apelin enhanced cell migration in a wound healing assay in a p38 MAPK-dependent manner. Furthermore, analysis of caspase-3 activation indicated that ATF4 knockdown up-regulated apelin expression, leading to the inability of MKK6 (CA) to exert pro-apoptotic effects. Taken together, our results suggest that ATF4-mediated repression of apelin contributes substantially to the pro-apoptotic effects of p38.
    APOPTOSIS 07/2014; · 3.61 Impact Factor
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    ABSTRACT: Effluent organic matter (EfOM) is the major cause of fouling in the low pressure membranes process for wastewater reuse. Coagulation and oxidation of biological wastewater treatment effluent have been applied for the fouling control of microfiltration membranes. However, the change in EfOM structure by pre-treatments has not been clearly identified. The changes of EfOM characteristics induced by coagulation and ozonation were investigated through size exclusion chromatography, UV/Vis spectrophotometry, fluorescence spectrophotometry and titrimetric analysis to identify the mechanisms in the reduction of ultrafiltration (UF) membrane fouling. The results indicated that reduction of flux decline by coagulation was due to modified characteristics of dissolved organic carbon (DOC) content. Total concentration of DOC was not reduced by ozonation. However, the mass fraction of the molecules with molecular weight larger than 5 kDa, fluorescence intensity, aromaticity, highly condensed chromophores, average molecular weight and soluble microbial byproducts decreased greatly after ozonation. These results indicated that EfOM was partially oxidized by ozonation to low molecular weight, highly charged compounds with abundant electron-withdrawing functional groups, which are favourable for alleviating UF membrane flux decline.
    Journal of Environmental Sciences 06/2014; 26(6):1325–1331. · 1.92 Impact Factor
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    ABSTRACT: The regulation of CCAAT/enhancer-binding protein-homologous protein (CHOP), an endoplasmic reticulum (ER) stress-response factor, is key to cellular survival. Hypoxia is a physiologically important stress that induces cell death in the context of the ER, especially in solid tumors. Although our previous studies have suggested that Cyclophilin B (CypB), a molecular chaperone, has a role in ER stress, currently, there is no direct information supporting its mechanism under hypoxia. Here, we demonstrate for the first time that CypB is associated with p300 E4 ligase, induces ubiquitination and regulates the proteasomal turnover of CHOP, one of the well-known pro-apoptotic molecules under hypoxia. Our findings show that CypB physically interacts with the N-terminal α-helix domain of CHOP under hypoxia and cooperates with p300 to modulate the ubiquitination of CHOP. We also show that CypB is transcriptionally induced through ATF6 under hypoxia. Collectively, these findings demonstrate that CypB prevents hypoxia-induced cell death through modulation of ubiquitin-mediated CHOP protein degradation, suggesting that CypB may have an important role in the tight regulation of CHOP under hypoxia.Cell Death and Differentiation advance online publication, 22 November 2013; doi:10.1038/cdd.2013.164.
    Cell death and differentiation 11/2013; · 8.24 Impact Factor
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    ABSTRACT: Cyclophilin, a cytosolic receptor for the immunosuppressive drug cyclosporin A, plays a role in diverse pathophysiologies along with its receptor, CD147. Although the interaction between cyclophilin A and CD147 is well established in inflammatory disease, that of cyclophilin B (CypB) with CD147 has not been fully explored, especially in cancer cell biology, and the exact molecular mechanism underlying such an association is poorly understood. In this study, we first identified high expression levels of CypB in 54 % of hepatocellular carcinoma patient tissues but in only 12.5 % of normal liver tissues. Then, we demonstrated that CypB overexpression protects human hepatoma cells against oxidative stress through its binding to CD147; this protective effect depends on the peptidyl prolyl isomerase activity of CypB. siRNA-mediated knockdown of CypB expression rendered hepatoma cells more vulnerable to ROS-mediated apoptosis. Furthermore, we also determined that a direct interaction between secreted CypB and CD147 regulates the extracellular signal-regulated kinase intracellular signaling pathway and is indispensible for the protective functions of CypB. For the first time, we demonstrated that CypB has an essential function in protecting hepatoma cells against oxidative stress through binding to CD147 and regulating the ERK pathway.
    Apoptosis 05/2012; 17(8):784-96. · 3.61 Impact Factor
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    ABSTRACT: Batch tests were carried out to evaluate the thermal treatment of low volatile organic compounds in low-permeability soil. The chemical oxidation by sodium persulfate catalyzed by heat and Fe (II) was evaluated. Enhanced persulfate oxidation of n-decane (C-10), n-dodecane (C-12), n-tetradecane (C-14), n-hexadecane (C-16), and phenanthrene was observed with thermal catalyst, indicating increased sulfate radical production. Slight enhancement of the pollutants oxidation was observed when initial sodium persulfate concentration increased from 5 to 50 g/L. However, the removal efficiency greatly decreased as soil/water ratio increased. It indicates that mass transfer of the pollutants as well as the contact between the pollutants and sulfate radical were inhibited in the presence of solids. In addition, more pollutants can be adsorbed on soil particles and soil oxidant demand increased when soil/water ratio becomes higher. The oxidation of the pollutants was significantly improved when catalyzed by Fe(II). The sodium persulfate consumption increased at the same time because the residual Fe(II) acts as the sulfate radical scavenger.
    Journal of Soil and Groundwater Environment. 04/2012; 17(2).
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    ABSTRACT: Synthetic and persistent endocrine disrupting chemicals (EDCs) such as 17α-ethinylestradiol (EE2) have been frequently detected in the effluent of wastewater treatment plants and induce hazards to humans and wildlife. In this study, biogenic Mn oxides were tested for the removal of EE2, and factors affecting the reaction were also investigated. The biogenic Mn oxides produced by Pseudomonas putida strain MnB1 were nano-sized and poorly crystallized particles. A concentration of 7.9 mg l−1 biogenic Mn oxides showed 87% EE2 (1 mg l−1) removal efficiency in 2 h, which confirms the excellent potential of biogenic Mn oxides for removal of estrogens. EE2 removal was enhanced at high Mn oxide doses and at low pH. Co-existing heavy metals significantly inhibit EE2 removal, due to their competition for the reactive sites of biogenic Mn oxides. Humic acid (HA) also obstructed EE2 removal, but the adverse effect was alleviated as HA concentration increased, possibly due to the formation of soluble complexes with the released Mn2+, of which adsorption onto Mn oxides reduces surface reactive sites.
    Water Air and Soil Pollution 01/2012; · 1.69 Impact Factor
  • Kwon Jeong, Hee-Man Kang, Seok-Oh Ko
    Journal of the Korean Society of Road Engineers. 06/2011; 13(2):187-193.

Publication Stats

3 Citations
21.36 Total Impact Points


  • 2012–2014
    • Kyung Hee University
      • • Department of Civil Engineering
      • • Department of Medicine
      Sŏul, Seoul, South Korea