J Park

Ewha Womans University, Sŏul, Seoul, South Korea

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Publications (4)3.81 Total impact

  • K H Song, J Park, H Ha
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    ABSTRACT: Diabetes, whether it occurs before or after transplantation, plays an important role to decrease graft function and survival. In addition renal lipid accumulation has been suggested to play a role in the development and progression of chronic renal allograft rejection. Intracellular lipid accumulation is governed by a balance between the influx and efflux of lipid. Cholesterol transporters, such as scavenger receptor (SR)-A1, CD36, and ATP binding cassette (ABC) A1 and G1 (ABCG1), coordinate to regulate cellular lipid status. Therefore, in the present study, we examined whether high glucose caused lipid accumulation in mesangial cells as a result of altered cholesterol transporters. Mouse mesangial cells were stimulated with 30 mmol/L D-glucose (high glucose); 100 μmol/L oleic acid (OA) used as a positive control. Cellular lipid accumulation was measured by Oil Red O staining. Protein and mRNA expression of cholesterol influx (SR-A1 and CD36) and efflux (ABCA1 and ABCG1) transporters were evaluated using Western blot analysis and real-time quantitative polymerase chain reaction, respectively. High glucose was shown to significantly increase lipid accumulation in mesangial cells at 24 hours as was observed for OA. SR-A1 and CD36 mRNA expression levels were 1.5-fold and 3.5-fold higher, respectively, in high glucose-stimulated than control mesangial cell, whereas ABCG1 mRNA expression decreased to 60% of controls; however, there was no decrease in ABCA1 mRNA. Altered protein expression of each transporter in mesangial cells cultured under conditions of high glucose concentrations was consistent with mRNA expression. Osmotic control using mannitol did not significantly affect any of the measured parameters in the present study. These results demonstrated that high glucose, in itself, can induce mesangial lipid accumulation; this effect may be associated with an impaired balance between the influx and efflux of cholesterol.
    Transplantation Proceedings 05/2012; 44(4):1021-5. DOI:10.1016/j.transproceed.2012.03.018 · 0.95 Impact Factor
  • J Park, K H Song, H Ha
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    ABSTRACT: Mesangial cell proliferation is one of the main features of chronic renal allograft rejection. One unique feature of fractalkine (CX3CL1) is its existence as both a membrane-tethered and a soluble form. Fractalkine expression is increased in acute and chronic allograft rejection. However, its role in mesangial cell proliferation has not yet been clearly explored. Thus, the present study examined whether fractalkine induced mesangial cell proliferation through production of reactive oxygen species (ROS) and activation of mitogen-activated protein kinase (MAPK), two known mediators of mesangial cell proliferation. Growth-arrested and synchronized mouse mesangial cells were stimulated with fractalkine in the presence versus absence of inhibitors against ROS, extracellular signal-regulated protein kinase (ERK), and p38 MAPK. Cell proliferation was assessed by methylthiazoletetrazolium assay, dichlorofluorescein (DCF)-sensitive cellular ROS production by a fluorometer, and MAPK activation by Western blot analysis. Fractalkine (10-50 ng/mL) significantly increased mesangial cell proliferation at 24 hours in a dose-dependent manner, an effect that was abrogated by the ROS and MAPK inhibitors. Fractalkine (50 ng/mL) also induced cellular ROS production and activation of ERK1/2 and p38 MAPK in mesangial cells. These results demonstrated that fractalkine can induce mesangial cell proliferation through production of cellular ROS and activation of MAPK.
    Transplantation Proceedings 05/2012; 44(4):1026-8. DOI:10.1016/j.transproceed.2012.03.045 · 0.95 Impact Factor
  • J Park, K H Song, H Ha
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    ABSTRACT: Fractalkine (CX3CL1) is a unique chemokine that functions not only as a chemokine but also as an adhesion molecule. Fractalkine plays an important role in the recruitment of macrophages into the kidneys by binding to its specific receptor CX3CR1, and renal fractalkine expression was shown to be increased in chronic renal allograft rejection. Considering that microcapillary inflammation is a key feature of chronic renal allograft rejection, the present study examined whether monocytes bind to mesangial cells cultured in the presence of lipopolysaccharide (LPS) through fractalkine/CX3CR1 in order to understand their regulation with respect to inflammation-induced renal allograft dysfunction. Mouse mesangial cells were stimulated with LPS in the presence or absence of fractalkine or CX3CR1 siRNA. Calcein-AM-labeled monocytes were used to evaluate monocyte binding. Fractalkine and CX3CR1 mRNA and protein expression were measured by real-time quantitative polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. LPS at 100 ng/mL significantly increased monocyte binding to mesangial cells. Each siRNA against fractalkine or CX3CR1 effectively inhibited LPS-induced monocyte-mesangial cell binding. Fractalkine and CX3CR1 mRNA expression were enhanced in mesangial cells stimulated with LPS. Fractalkine protein synthesis in media and lysate of mesangial cells were also induced by LPS. These results demonstrated that LPS induces monocyte-mesangial cell binding through the fractalkine/CX3CR1 system and suggested that fractalkine/CX3CR1 system may contribute to renal inflammation leading to chronic renal allograft rejection.
    Transplantation Proceedings 05/2012; 44(4):1029-31. DOI:10.1016/j.transproceed.2012.03.046 · 0.95 Impact Factor
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    ABSTRACT: Tubulointerstitial fibrosis, which is characterized by the progressive accumulation of extracellular matrix (ECM), is the main feature of chronic renal allograft dysfunction. Transforming growth factor-β1 (TGF-β1) is the key inducer of tubulointerstitial fibrosis. Plasminogen activator inhibitor-1 (PAI-1), a major inhibitor of ECM degradation, is increasingly recognized to play an important role in renal fibrosis. ECM accumulation is the net result of ECM synthesis and degradation. We previously reported that reactive oxygen species (ROS) and subsequent activation of mitogen-activated protein kinase (MAPK) are required for the TGF-β1-induced epithelial-to-mesenchymal transition in renal proximal tubular epithelial cells. In the present study, we examined the role of the ROS-MAPK pathways in TGF-β1-induced fibronectin and PAI-1 up-regulation in renal tubular epithelial cells. Growth arrested, synchronized normal rat kidney epithelial (NRK-52E) cells were stimulated with TGF-β1 (0.2-20 ng/mL) or H(2)O(2) (1-500 μmol/L) in the presence or absence of inhibitors of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (diphenyleneiodonium [DPI] and apocynin [Apo]) and MAPK (PD98059, an MEK inhibitor, or a p38 MAPK inhibitor) for up to 48 hours. Both TGF-β1 and H(2)O(2) increased fibronectin and PAI-1 secretion in dose-dependent manners. Chemical inhibition of NADPH oxidase, extracellular signal-regulated kinase (ERK), or p38 MAPK all inhibited TGF-β1-induced and H(2)O(2)-induced fibronectin and PAI-1 up-regulation. These results suggested that NADPH oxidase-mediated ROS and subsequent ERK and p38 MAPK activation play important roles in ECM accumulation in the renal tubulointerstitium.
    Transplantation Proceedings 04/2012; 44(3):625-8. DOI:10.1016/j.transproceed.2011.12.054 · 0.95 Impact Factor