Eun Kyoung Kim

Wonkwang University, Riri, North Jeolla, South Korea

Are you Eun Kyoung Kim?

Claim your profile

Publications (50)162.66 Total impact

  • Eun Kyoung Kim, Joo-Yong Hahn, Young Bin Song, Sang-Chol Lee, Jin-Ho Choi, Seung-Hyuk Choi, Sang Hoon Lee, Yeon Hyeon Choe, Hyeon-Cheol Gwon
    [Show abstract] [Hide abstract]
    ABSTRACT: In the effects of postconditioning on myocardial reperfusion in patients with ST-segment elevation myocardial infarction (POST) trial, ischemic postconditioning did not improve myocardial reperfusion in 700 patients with STEMI undergoing primary PCI. However, the impact of postconditioning on myocardial salvage and infarct size still needs to be addressed. The aim of this study was to investigate the effect of ischemic postconditioning on myocardial salvage using cardiac magnetic resonance (CMR) in patients with STEMI undergoing primary PCI. For the CMR substudy, a total of 111 patients was analyzed, 56 in the postconditioning group and 55 undergoing conventional primary PCI in the control group. Postconditioning was performed immediately after restoration of coronary flow by four cycles of 1-min balloon occlusion separated by 1 min of deflation. The primary end point was myocardial salvage measured by CMR 3 days after the index event. The myocardial salvage index was not improved by ischemic postconditioning compared with conventional PCI (46.3 ± 18.5 vs. 45.7 ± 20.5 %, p = 0.86). The infarct size was not significantly different between the two groups (18.8 ± 10.3 vs. 20.2 ± 11.0 %, p = 0.52). Moreover, there was no significant difference in the rates of microvascular obstruction or hemorrhagic infarction between the groups. CMR study demonstrated that ischemic postconditioning during primary PCI in STEMI patients did not improve myocardial salvage or reduce infarct size. These findings further support the results of the POST trial which showed no benefit of ischemic postconditioning as an adjunctive treatment of primary PCI.
    The international journal of cardiovascular imaging. 01/2015;
  • [Show abstract] [Hide abstract]
    ABSTRACT: mTORC1 plays a key role in autophagy as a negative regulator. The currently known targets of mTORC1 in the autophagy pathway mainly function at early stages of autophagosome formation. Here, we identify that mTORC1 inhibits later stages of autophagy by phosphorylating UVRAG. Under nutrient-enriched conditions, mTORC1 binds and phosphorylates UVRAG. The phosphorylation positively regulates the association of UVRAG with RUBICON, thereby enhancing the antagonizing effect of RUBICON on UVRAG-mediated autophagosome maturation. Upon dephosphorylation, UVRAG is released from RUBICON to interact with the HOPS complex, a component for the late endosome and lysosome fusion machinery, and enhances autophagosome and endosome maturation. Consequently, the dephosphorylation of UVRAG facilitates the lysosomal degradation of epidermal growth factor receptor (EGFR), reduces EGFR signaling, and suppresses cancer cell proliferation and tumor growth. These results demonstrate that mTORC1 engages in late stages of autophagy and endosome maturation, defining a broader range of mTORC1 functions in the membrane-associated processes. Copyright © 2015 Elsevier Inc. All rights reserved.
    Molecular cell. 12/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Regulation of VSMC phenotype by extracellular matrix.
    Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 11/2014; · 5.09 Impact Factor
  • Circulation 08/2014; 130(6):e54-5. · 14.95 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Although obesity is a risk factor for cardiovascular disease and mortality, several studies have reported that patients with obesity who have suffered acute myocardial infarction or have undergone percutaneous coronary intervention (PCI) have better clinical outcomes than their normal weight counterparts. We evaluated the impact of overweight on myocardial infarct size in patients undergoing primary PCI for ST-segment elevation myocardial infarction (STEMI).
    Atherosclerosis 06/2014; 235(2):570-575. · 3.71 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: During the pathogenesis of atherosclerosis, adhesion of monocytes to vascular endothelium and subsequent migration across the endothelium has been recognized as a key process in the chronic inflammatory response in atherosclerosis. As type 2 diabetes is closely associated with the pathogenesis of atherosclerosis, we investigated whether monocyte adhesion and migration were affected by insulin. We found that insulin activated Akt and induced subsequent migration in THP-1. However, glucose and IGF-1, which is a growth factor that is structurally similar to insulin, were not effective. Insulin-dependent migration of THP-1 was blocked by inhibition of PI3K or Akt and by silencing of Akt1. Insulin-dependent migration of BDMCs was attenuated by inhibition of PI3K and Akt. In addition, BDMCs from Akt1(-/-) mice showed defects in insulin-dependent migration. Stimulation of THP-1 with insulin caused adhesion with HUVECs that was blocked by silencing of Akt1. However, stimulation of HUVECs did not cause adhesion with THP-1. Moreover, BDMCs from Akt1(-/-) mice showed defects in insulin-dependent adhesion with HUVECs. Insulin induced surface expression of Mac-1, and neutralization of Mac-1 blocked insulin-induced adhesion of THP-1 as well as BDMCs. Surface expression of Mac-1 was blocked in THP-1 with silenced Akt1, and in BDMCs isolated from mice lacking Akt1. Finally, trans-endothelial migration of THP-1 and BDMCs was blocked by Mac-1-neutralizing antibody, in THP-1 with silenced Akt1 and in BDMCs from Akt1(-/-) mice. These results suggest that insulin stimulates monocyte trans-endothelial migration through Akt-dependent surface expression of Mac-1, which may be part of the atherogenesis in type 2 diabetes.
    Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 06/2014; · 5.09 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Polyunsaturated fatty acids (PUFAs) have important pharmacological effects on mammalian cells. Here, we show that carboxyl group-containing PUFAs inhibit lysophosphatidic acid (LPA)-induced focal adhesion formation, thereby inhibiting migration and adhesion. Carboxyl group-containing PUFAs inhibit LPA-induced calcium mobilization, whereas ethyl ester-group containing PUFAs have no effect. In addition, carboxyl group-containing PUFAs functionally inhibit LPA-dependent RhoA activation. Given these results, we suggest that PUFAs may inhibit LPA-induced calcium/RhoA signaling pathways leading to focal adhesion formation. Carboxyl group-containing PUFAs may have a functional role in this regulatory mechanism.
    FEBS Letters 06/2014; · 3.34 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: High dose rosuvastatin loading before percutaneous coronary interventions (PCI) reduces the myocardial damage and the incidence of adverse cardiac events in patients with stable angina and acute coronary syndrome. However, no studies are present yet about rosuvastatin loading in patients with ST-segment elevation myocardial infarction (STEMI) in a primary PCI setting. A total of 475 patients who underwent primary PCI for STEMI were studied. The study population was divided into two groups with 208 patients in the statin group=40 mg rosuvastatin loading before primary PCI and 267 patients in the control group=no statin pretreatment. At median 3 days after PCI a single-photon emission computed tomography (SPECT) was performed with technetium 99m tetrofosmin For this study were compared infarct size, corrected Thrombolysis in Myocardial Infarction (TIMI) frame count and the myocardial blush grade (MBG) between the both groups. Baseline clinical and procedural characteristics were similar between the groups. Infarct size, as assessed by SPECT, was significantly smaller (19.0±15.9% vs. 22.9±16.5%, p=0.009) in the statin group than in the control group. Patients of the statin group showed a lower corrected TIMI frame count (28.2±19.3 vs. 32.6±21.4, p=0.020), and higher MBG (2.49±0.76 vs. 2.23±0.96, p=0.001) than the patients of the control group. The multivariate analysis revealed that rosuvastatin loading {odds ratio (OR) 0.61}, pain to balloon time (OR 2.05), anterior myocardial infarction (OR 3.89) and final the MBG (OR 2.93) were independent predictors of a large infarct size. A high dose rosuvastatin loading before the primary PCI reduced the infarct size by microvascular myocardial perfusion improvement.
    Korean Circulation Journal 03/2014; 44(2):76-81.
  • Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 01/2014; · 5.09 Impact Factor
  • Eun Kyoung Kim, Seok Joon Kong, Sung Kun Chung
    [Show abstract] [Hide abstract]
    ABSTRACT: The aim was to compare the effect of subconjunctival injections of ranibizumab and bevacizumab on corneal neovascularization (NV) in rabbits. NV was induced by placing a suture at the corneal periphery of rabbits (n = 30 eyes). Immediately after suturing, the rabbits were divided into 3 groups and 7 days later administered subconjunctival injections of ranibizumab (Lucentis; 0.5 mg/0.05 mL), bevacizumab (Avastin; 5 mg/0.05 mL), or normal saline (control), respectively. The time-course photographs to measure the area of the corneal NV were obtained on days 7, 10, and 14 after suture placement. Histological examination and immunohistochemical analysis for the vascular endothelial growth factor and CD34 were performed. Analysis of digital photographs showed that there was less corneal NV in the ranibizumab- and bevacizumab-treated eyes than in the control eyes (P = 0.012, 1-way analysis of variance); however, no significant differences between the ranibizumab- and bevacizumab-treated eyes were seen. In addition, there was less staining for vascular endothelial growth factor and CD34 in the corneas from the ranibizumab-treated eyes and bevacizumab-treated eyes than in the control eyes, and there were no significant differences in the staining intensity between the ranibizumab- and bevacizumab-treated eyes. Subconjunctival ranibizumab and bevacizumab injections were not associated with any complications during observations. Subconjunctival administrations of ranibizumab or bevacizumab inhibit corneal NV in rabbits and have equivalent effects on it.
    Cornea 11/2013; · 1.75 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Ischemic postconditioning has been reported to reduce infarct size in patients with ST-segment elevation myocardial infarction (STEMI). However, cardioprotective effects of postconditioning have not been demonstrated in a large-scale trial. We performed a multicenter, prospective, randomized, open-label, blinded endpoint trial. A total of 700 patients undergoing primary percutaneous coronary intervention (PCI) for STEMI within 12 hours after symptom onset were randomly assigned to the postconditioning group or the conventional primary PCI group in a 1:1 ratio. Postconditioning was performed immediately after restoration of coronary flow as follows: the angioplasty balloon was positioned at the culprit lesion, and inflated 4 times for 1 minute with low-pressure (< 6 atm) inflations, each separated by 1 minute of deflation. The primary endpoint was complete ST-segment resolution (the percentage resolution of ST-segment elevation >70%) measured at 30 minutes after PCI. Complete ST-segment resolution occurred in 40.5% of patients in the postconditioning group and 41.5% of patients in the conventional PCI group (absolute difference, -1.0%; 95% confidence interval, -8.4% to 6.4%; P=0.79). The rate of myocardial blush grade of 0 or 1 and the major adverse cardiac events (a composite of death, myocardial infarction, severe heart failure, or stent thrombosis) at 30 days did not differ significantly between the postconditioning group and the conventional PCI group (17.2% versus 22.4%, P=0.20, and 4.3% versus 3.7%, P=0.70, respectively). Ischemic postconditioning did not improve myocardial reperfusion in patients with STEMI undergoing primary PCI with current standard practice. Identifier: NCT00942500.
    Circulation 09/2013; · 14.95 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Platelet-activating factor (PAF), 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine, is a potent phospholipid mediator and has been reported to be localized in atherosclerotic plaque. However, its role in the progression of atherosclerosis remains unclear. In the present study, we investigated the role of PAF in the production of matrix metalloproteinase (MMP) in primary vascular smooth muscle cells (VSMCs). When rat aortic primary VSMCs were stimulated with PAF (1 nmol/L), the expressions of MMP-2 mRNA and protein, but not of MMP-9, were significantly increased, and these up-regulations were markedly attenuated by inhibiting extracellular signal-regulated kinases (ERK) using molecular and pharmacological inhibitors, but not by using inhibitors of p38 mitogen-activated protein kinase or c-Jun N-terminal kinase. Likewise, ERK phosphorylation was markedly enhanced in PAF-stimulated VSMCs, and this was attenuated by WEB2086, but not by EGF receptor inhibitor, demonstrating the specificity of PAF receptor in PAF-induced ERK phosphorylation. In immunofluorescence studies, β-arrestin2 in PAF-stimulated VSMCs colocalized with PAF receptor and phosphorylated ERK (P-ERK). Co-immunoprecipitation results suggest that β-arrestin2-bound PAF receptors existed as a complex with P-ERK. In addition, PAF-induced ERK phosphorylation and MMP-2 production were significantly attenuated by β-arrestin2 depletion. Taken together, the study shows that PAF enhances MMP-2 production in VSMCs via a β-arrestin2-dependent ERK signaling pathway.
    The Journal of Lipid Research 08/2013; · 4.73 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Among the parameters for surveillance of patients at risk of acute type A aortic dissection, the aortic size has been considered a cardinal factor. Preventive surgery of the aorta in asymptomatic patients on the basis of size alone is still controversial in patient populations lacking other risk factors for aortic dissection. The aim of the present study was to assess the value of the aortic diameter as a current criterion for elective aortic surgery to prevent the development of aortic dissection in patients without and with Marfan syndrome (MFS). We reviewed the data from patients diagnosed with acute type A aortic dissection from December 1994 to March 2009 at our institute. A total of 237 patients who presented with acute type A aortic dissection were enrolled, of whom 31 were diagnosed with MFS. The maximal ascending aorta size was 46.7 mm (range, 42.9-51.6) in non-MFS patients and 58.5 mm (range, 43.8-64.9) in MFS patients (P < .001). Two thirds (74%) of the MFS patients had a maximal aortic root size of ≥45 mm. However, 87% of the 206 non-MFS patients had an aortic diameter <55 mm. Non-MFS patients presenting with an aortic size <55 mm developed aortic dissection at a younger age and had a higher body mass index than those with an aortic size ≥55 mm. Type A aortic dissection occurs in smaller aortas in non-MFS patients compared with those with MFS.
    The Journal of thoracic and cardiovascular surgery 07/2013; · 3.41 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The aim of this study was to determine the normal values for aortic pulse wave velocity (PWV) and distensibility using cine and phase contrast cardiac magnetic resonance imaging (CMRI) in patients without cardiovascular risk factors. PWV and distensibility are indispensible predictors of global and regional cardiovascular risk. Regional heterogeneity in aortic stiffness plays an important role in the pathogenesis of cardiovascular disease. Contrary to global estimates of aortic PWV that are commonly measured with tonometry, CMRI has emerged as an important method for estimating regional PWV and distensibility. A total of 124 Korean patients, aged 20-79 years and free of cardiovascular risk factors, were categorized by age decade. Using cine and phase contrast sequences, the cross-sectional area for distensibility and average blood flow were measured at four aortic levels: the ascending, upper descending thoracic, lower thoracic and abdominal aorta. Regional PWV was determined in four aortic segments: proximal, descending thoracic, abdominal aorta and across the entire aorta. Distensibility at the four levels of the aorta from the ascending to distal (4.4 ± 2.5, 4.0 ± 1.6, 5.2 ± 1.9, and 3.3 ± 1.7 × 10(-3) mm/Hg, respectively) was higher in women (P < 0.001) and decreased with age. The regional PWV was highest in the descending thoracic aorta and increased with age. The present study is the first to show the heterogeneity in aortic PWV and distensibility, as well to provide normal values for these parameters using CMRI in an Asian sample.
    The international journal of cardiovascular imaging 03/2013; · 2.15 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Peripheral artery disease (PAD) is an important marker for the risk stratification of patients with coronary artery disease (CAD). We investigated the prevalence of PAD in patients undergoing percutaneous coronary intervention (PCI) with CAD and the relationship between ankle-brachial pressure index (ABPI) and CAD severity. A total of 711 patients undergoing PCI for CAD from August 2009 to August 2011 were enrolled. PAD diagnosis was made using the ABPI. The prevalence of PAD was 12.8%. In PAD patients, mean values of right and left ABPI were 0.71 ± 0.15 and 0.73 ± 0.15. Patients with PAD had a higher prevalence of left main coronary disease (14.3% vs 5.8%, P = 0.003), more frequently had multivessel lesions (74.9% vs 52.1%, P < 0.001) and had higher SYNTAX score (18.2 ± 12.3 vs 13.1 ± 8.26, P = 0.002). Using multivariate analysis, we determined that left main CAD (OR, 2.954; 95% CI, 1.418-6.152, P = 0.004) and multivessel CAD (OR, 2.321; 95% CI, 1.363-3.953, P = 0.002) were both independently associated with PAD. We recommend that ABPI-based PAD screening should be implemented in all patients undergoing PCI with CAD, especially in severe cases.
    Journal of Korean medical science 01/2013; 28(1):87-92. · 0.84 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: A 22-year-old man was referred to our institution due to lower back pain and was diagnosed with Langerhans cell histiocytosis of the thoracic and lumbar spine. The patient achieved complete remission with radiotherapy and chemotherapy. One year later, right cervical lymphadenopathy was observed and Hodgkin's lymphoma was confirmed on biopsy. The patient was treated with chemotherapy and autologous stem cell transplantation, and experienced no further symptoms. Further, no evidence of recurrence was observed on follow-up imaging. This report discusses the association between Langerhans cell histiocytosis and Hodgkin's lymphoma.
    The Korean Journal of Internal Medicine 12/2012; 27(4):459-62.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Acanthopanax senticosus (Rupr. & Maxim.) Harms (AS) has been used as a traditional medicine for the treatment of hypertension, rheumatism, ischemic heart disease, diabetes, and hepatitis in East Asia. This herb has been reported to possess anti-cancer, anti-diabetes, and anti-inflammatory properties. To examine the anti-inflammatory activity of AS extract (ASE) and its mechanism of action in Porphyromonas gingivalis lipopolysaccharide (P. gingivalis LPS)-stimulated macrophages. P. gingivalis LPS was used to induce an inflammatory response in the murine macrophage cell line RAW 264.7. Pro-inflammatory cytokines were measured by using an enzyme-linked immunosorbent assay. We used western blot assays and real-time quantitative polymerase chain reaction to detect protein and mRNA expression, respectively. Luciferase assays were performed to determine the transactivity of transcription factors. Nuclear translocation of nuclear factor (NF)-κB was assessed by confocal microscopy. ASE significantly induced the expression and activity of heme oxygenase-1 (HO-1), which is known to produce an anti-inflammatory effect, in RAW 264.7 cells, through NF-E2-related factor 2 (Nrf-2), Janus kinase, and extracellular signal-regulated kinase activation. ASE also effectively suppressed the production of pro-inflammatory cytokines, tumor necrosis factor α, interleukin (IL)-1β, and IL-6, and decreased the nuclear translocation and transactivity of activator protein-1 (AP-1) and NF-κB by inhibiting the phosphorylation of IκB-α in P. gingivalis LPS-stimulated macrophage cells. Furthermore, ASE inhibits signal transducer and activator of transcription (STAT)1 phosphorylation while it activates STAT3 phosphorylation in P. gingivalis LPS-stimulated RAW 264.7 cells. Our study suggests that ASE produces anti-inflammatory effects on P. gingivalis LPS-stimulated macrophages through a reduction in AP-1 and NF-κB activity, modulation of STAT1 and STAT3 phosphorylation, and upregulation of HO-1 expression through the activation of mitogen-activated protein kinase and Nrf-2 signaling pathways. Therefore, ASE could be a candidate for the prevention and treatment of periodontal diseases that involve excessive inflammation.
    Journal of ethnopharmacology 06/2012; 142(3):819-28. · 2.32 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: A 29-year-old pregnant woman with recurrent pericardial effusion and a cardiac tumor, diagnosed as an angiosarcoma, was treated with surgical resection of the tumor followed by radiotherapy. Immediately after completion of radiotherapy, she developed bilateral breast masses, which were also confirmed as angiosarcomas. We thought this might be the first case of bilateral angiosarcoma of the breast metastasizing to heart mimicking a primary cardiac angiosarcoma, although we could not conclude with certainty that angiosarcoma of the heart was not the primary site.
    The Korean Journal of Internal Medicine 06/2012; 27(2):224-8.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The etiology of acute pericarditis is often thought to be autoimmune, and Graves' disease has been reported in a few series to manifest as acute pericarditis. Since the etiology of recurrent pericarditis is known to be more associated with autoimmune causes, recurrent acute pericarditis may be a potential cardiovascular complication of Graves' disease. We report a case of recurrent acute pericarditis that was presumed to be associated with Graves' disease which was controlled after management of the problem of the thyroid.
    Korean Circulation Journal 06/2012; 42(6):419-22.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Phosphatidylinositol 3-kinase (PI3K) is essential for both G protein-coupled receptor (GPCR)- and receptor tyrosine kinase (RTK)-mediated cancer cell migration. Here, we have shown that maximum migration is achieved by full activation of phosphatidylinositol 3,4,5-trisphosphate-dependent Rac exchanger 1 (P-Rex1) in the presence of Gβγ and PI3K signaling pathways. Lysophosphatidic acid (LPA)- induced migration was higher than that of epidermal growth factor (EGF)-induced migration; however, LPA-induced activation of Akt was lower than that stimulated by EGF. LPA-induced migration was partially blocked by either Gβγ or RTK inhibitor and completely blocked by both inhibitors. LPA-induced migration was synergistically increased in the presence of EGF and vice versa. In correlation with these results, sphingosine-1-phosphate (S1P)-induced migration was also synergistically induced in the presence of insulin-like growth factor-1 (IGF-1). Finally, silencing of P-Rex1 abolished the synergism in migration as well as in Rac activation. Moreover, synergistic activation of MMP-2 and cancer cell invasion was attenuated by silencing of P-Rex1. Given these results, we suggest that P-Rex1 requires both Gβγ and PI3K signaling pathways for synergistic activation of Rac, thereby inducing maximum cancer cell migration and invasion.
    Experimental and Molecular Medicine 05/2012; 44(8):483-91. · 2.46 Impact Factor

Publication Stats

239 Citations
162.66 Total Impact Points


  • 2014
    • Wonkwang University
      Riri, North Jeolla, South Korea
  • 2011–2014
    • Sungkyunkwan University
      • School of Medicine
      Sŏul, Seoul, South Korea
    • Ajou University
      • Department of Endocrinology and Metabolism
      Seoul, Seoul, South Korea
    • Kwandong University
      • College of Medicine
      Gangneung, Gangwon, South Korea
  • 2011–2013
    • Catholic University of Korea
      • • Department of Ophthalmology
      • • College of Medicine
      Sŏul, Seoul, South Korea
  • 2009–2012
    • Ulsan University Hospital
      Urusan, Ulsan, South Korea
    • Pusan National University
      • • Department of Pharmacology
      • • Department of Thoracic and Cardiovascular Surgery
      Pusan, Busan, South Korea
  • 2010
    • Korea University
      • Department of Psychology
      Sŏul, Seoul, South Korea
  • 2008
    • Kyung Hee University
      • College of Oriental Medicine
      Seoul, Seoul, South Korea