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( Eun Ju Cho ),( Jeong Hoon Lee ),( Il Young Lee ),( Moon Young Kim ),( Jeong Ju Yoo ),( Won Mook Choi ),( Young Youn Cho ),( Min Jong Lee ),( Yuri Cho ),( Dong Hyeon Lee ),( Yun Bin Lee ),( Su Jong Y 대한간학회 2013 춘·추계 학술대회 (KASL) Vol.2013 No.1
Background: Hepatic venous pressure gradient (HVPG) is the gold standard for assessing portal pressure. In this study, we investigated which noninvasive fibrosis test most effectively reflects HVPG and predicts prognosis in patients with alcoholic liver disease (ALD). Methods: A total of 195 consecutive patients with ALD were included. Biochemical indices and liver stiffness assessed by transient elastography (TE) were compared with HVPG. Results: During a median follow-up period of 23.1 months, 51 patients died, including 21 liver-related deaths. The diagnostic values of liver stiffness in detecting clinically significant portal hypertension (CSPH; HVPG≥10 mmHg) was significantly higher (AUROC=0.87±0.03) than those of biochemical indices (i.e. APRI, FIB4, P2/MS and platelet count/spleen diameter ratio; all P<0.001). In multivariate analysis, liver stiffness was most significantly correlated to HVPG (P<0.001), whereas other biochemical indices were not. On the other hand, the prognostic values of liver stiffness for liver-related death (AUROC= 0.73±0.07) did not differ from those of FIB4 (0.78±0.04), HVPG (0.70±0.07) and APRI (0.69±0.04). In multivariate analysis, significant risk factors for liver-related death were Child score (hazard ratio [HR]=2.35, P<0.001), varices >F2 (HR=5.85; P=0.002) and FIB4 (HR=1.11, P=0.03), but not liver stiffness and HVPG. For all-cause death, age and FIB4 were independent predictors in compensated patients (P=0.02 and <0.001, respectively), whereas Child score was in decompensated patients (P<0.001). Conclusions: In patients with ALD, liver stiffness most accurately predicts CSPH, but did not improve the prognostic values of traditional risk factors for mortality, whereas FIB4 was independent predictor for liver disease-related death and allcause death.
Effect of crotonaldehyde on the induction of HO-1 expression in A549 cells
Seung Eun Lee,Hye Rim Park,Hong Duck Yun,Hyemi Kim,진영호,Cheung-Seog Park,Hyun-Jong Ahn,JeongJeCho,Yong Seek Park,Y. S. Park 대한독성 유전단백체 학회 2017 Molecular & cellular toxicology Vol.13 No.2
Cigarette smoke contains approximately 5,000 chemical components, including reactive chemicals and free radicals that are associated with an increased risk of chronic obstructive pulmonary disease (COPD). Cigarette smoke is also known to promote inflammation as part of various inflammatory airway diseases. Crotonaldehyde (CRA) is a highly toxic α, β-unsaturated aldehyde that is a major component of cigarette smoke. Exposure to CRA has been previously shown to result in adverse effects on respiratory health. Heme oxygenase-1 (HO-1) is an inducible enzyme that is activated by various stress-inducing stimuli to perform a diverse range of physiological functions, including anti-oxidant, anti-apoptotic, and anti-inflammatory effects. The present study aimed to investigate the effect of CRA stimulation on HO-1 expression in human lung adenocarcinoma epithelial (A549) cells. Stimulation of cells with CRA was shown to result in upregulated HO-1 expression via the induction of nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation, and activation of the p38 mitogen-activated protein kinase (MAPK) pathway. Furthermore, zinc protoporphyrin (ZnPP; a specific HO-1 inhibitor) was used to inhibit HO-1 activity, and this was shown to cause a significant increase in the rate of apoptosis of CRAexposed cells. Taken together, these results suggest that HO-1 exerts an anti-apoptotic effect in CRA-exposed human lung adenocarcinoma epithelial cells, and thus protects cells against CRA-induced oxidative stress.
등골나물 추출물이 인간의 유방암세포인 MDA-MB-231 세포의 이동, 침윤 및 부착에 미치는 영향
우은영(Eun Young Woo),박소영(So Young Park),권수진(Soo Jin Kwon),권규택(Gyoo Taik Kwon),김종대(Jong Dae Kim),임순성(Soon Sung Lim),윤정한(Jung H.Y. Park) 한국식품과학회 2011 한국식품과학회지 Vol.43 No.2
등골나물은 국화과 여러해살이 식물로 한방에서는 고혈압, 폐렴, 황달, 홍역, 요통 등에 사용한다고 알려져 있다. 본 연구에서는 등골나물의 꽃 부위를 추출하여 등골나물 추출물이 유방암 세포인 MDA-MB-231 세포의 이동, 침윤 및 부착에 미치는 영향을 조사하였다. 그 결과 MDA-MB-231 세포의 이동, 침윤 및 부착은 등골나물 추출물의 농도(0-20 μg/mL)가 증가할수록 현저하게 감소하였다. 등골나물 추출물은 MMP-9, MMP-2의 활성을 억제하였고, TIMP-1의 발현은 감소시킨 반면 TIMP-2의 발현은 증가시켰다. 또한, 등골나물 추출물은 uPA, VEGF 그리고 ICAM의 mRNA 및 단백질 수준을 현저히 감소시켰다. 특히, 등골나물 헥산 분획물이 유방암세포의 이동을 현저하게 억제하였다. 이상의 결과로부터 등골나물 추출물은 MMP-9, MMP-2, uPA, TIMP-1 및 ICAM의 감소, TIPM-2의 증가를 통해 유방암세포의 전이를 억제하는 것으로 판단된다. 따라서 본 연구는 이러한 효능을 지닌 등골나물 추출물을 암전이에 효과가 있는 암예방제나 항암제로 개발할 수 있는 가능성을 제시한다. The metastatic effect of Eupatorium japonicum extract (EJE) on MDA-MB-231 human breast cancer cells was investigated. MDA-MB-231 cells were treated with various concentrations of EJE (0, 5, 10 and 20 μg/mL). EJE inhibited cell migration, invasion and adhesion of MDA-MB-231 cells in dose-dependent manners. Gelatin zymography exhibited that EJE significantly down regulated secretion of matrix metalloproteinase (MMP)-9 and MMP-2. EJE decreased the protein levels of tissue inhibitor of metalloproteinase (TIMP)-1 but increased TIMP-2 levels. Additionally, EJE reduced the protein and mRNA levels of urokinase-type plasminogen activator (uPA), vascular endothelial growth factor (VEGF) and intercellular adhesion molecule (ICAM). In several solvent fractions of EJE, the hexane fraction markedly decreased MDAMB-231 cell migration. Thus, these finding suggest that EJE may be a potential antimetastatic agent, which can considerably inhibit the metastatic and invasive capacity of breast cancer cells.
Effect of crotonaldehyde on the induction of COX-2 expression in human endothelial cells
Seung Eun Lee,Hye Rim Park,Hyemi Kim,Yeoum Choi,Young-Ho Jin,Cheung-Seog Park,Hyun-Jong Ahn,Jeong-Je Cho,Yong Seek Park,Y. S. Park 대한독성 유전단백체 학회 2017 Molecular & cellular toxicology Vol.13 No.3
Cyclooxygenase-2 (COX-2), an inducible isoform protein, regulates diverse biological actions in vascular pathophysiology. COX-2 is induced in response to numerous stimuli, which results in prostaglandin (PG) production related to inflammation. Crotonaldehyde (CRA) is an extremely toxic α, β-unsaturated aldehyde and a major compound found in cigarette smoke. α, β-Unsaturated aldehyde in cigarette smoke is thought to mediate inflammation and vascular dysfunction. In this study, we evaluated the effect of CRA stimulation on COX-2 expression in human umbilical vein endothelial cells. CRA-stimulated COX-2 induction was accompanied by enhanced p38 phosphorylation and PGE2 generation. However, CRA-induced PGE2 production was reduced by pretreatment with an inhibitor of p38 MAPK. These results demonstrated that in human endothelial cells, CRA-induced COX-2-dependent PGE2 generation was mediated by p38 MAPK, and CRA may play a role in the development of inflammation.
H-Ras is degraded by Wnt/beta-catenin signaling via beta-TrCP-mediated polyubiquitylation.
Kim, Sung-Eun,Yoon, Ju-Yong,Jeong, Woo-Jeong,Jeon, Soung-Hoo,Park, Yoon,Yoon, Jong-Bok,Park, Y N,Kim, Hoguen,Choi, Kang-Yell Cambridge University Press 2009 Journal of cell science Vol.122 No.6
<P>Ras is an important proto-protein that is regulated primarily by GDP/GTP exchange. Here, we report a novel regulatory mechanism whereby turnover of both endogenous and overexpressed H-Ras protein is controlled by beta-TrCP-mediated ubiquitylation, proteasomal degradation and the Wnt/beta-catenin signaling pathway. The interaction of H-Ras with the WD40 domain of beta-TrCP targeted H-Ras for polyubiquitylation and degradation. This process was stimulated by Axin or adenomatous polyposis coli (Apc), and was inhibited by Wnt3a. Ras-mediated cellular transformation was also inhibited by the expression of beta-TrCP and/or Axin. In vivo regulation of Ras stability by Wnt/beta-catenin signaling was determined via measurements of the status of Ras in the intestines of mice stimulated with recombinant Wnt3a by intravenous tail vein injection. The regulation of Ras stability by Wnt/beta-catenin signaling provides a mechanical basis for crosstalk between the Wnt/beta-catenin and the Ras-ERK pathways involved in transformation.</P>
Cheon, So Y.,Cho, Kyoung J.,Kim, So Y.,Kam, Eun H.,Lee, Jong E.,Koo, Bon-Nyeo Frontiers Media S.A. 2016 Frontiers in cellular neuroscience Vol.10 No.-
<P>Conditions of increased oxidative stress including cerebral ischemia can lead to blood–brain barrier dysfunction via matrix metalloproteinase (MMP). It is known that MMP-9 in particular is released from brain endothelial cells is involved in the neuronal cell death that occurs after cerebral ischemia. In the intracellular signaling network, apoptosis signal-regulating kinase 1 (ASK1) is the main activator of the oxidative stress that is part of the pathogenesis of cerebral ischemia. ASK1 also promotes apoptotic cell death and brain infarction after ischemia and is associated with vascular permeability and the formation of brain edema. However, the relationship between ASK1 and MMP-9 after cerebral ischemia remains unknown. Therefore, the aim of the present study was to determine whether blocking ASK1 would affect MMP-9 activity in the ischemic brain and cultured brain endothelial cells. Our results showed that ASK1 inhibition efficiently reduced MMP-9 activity <I>in vivo</I> and <I>in vitro</I>. In endothelial cell cultures, ASK1 inhibition upregulated phosphatidylinositol 3-kinase/Akt/nuclear factor erythroid 2 [NF-E2]-related factor 2/heme oxygenase-1 signals and downregulated cyclooxygenase-2 signals after hypoxia/reperfusion. Additionally, in neuronal cell cultures, cell death occurred when neurons were incubated with endothelial cell-conditioned medium (EC-CM) obtained from the hypoxia/reperfusion group. However, after incubation with EC-CM and following treatment with the ASK1 inhibitor NQDI-1, neuronal cell death was efficiently decreased. We conclude that suppressing ASK1 decreases MMP-9 activity in brain endothelial cells, and leads to decreased neuronal cell death after ischemic injury.</P>
Park, Jung-Eun,Kim, Sang-Mi,Oh, Jong-K.,Kim, Jin-Y.,Yoon, Sung-Soo,Lee, Dong-Soon,Kim, Young-Soo Korean Society for Biochemistry and Molecular Biol 2005 Journal of biochemistry and molecular biology Vol.38 No.6
Resistance to imatinib mesylate (also known as Gleevec, Glivec, and STI571) often becomes a barrier to the treatment of chronic myelogenous leukemia (CML). In order to identify markers of the action of imatinib mesylate, we used a mass spectrometry approach to compare protein expression profiles in human leukemia cells (K562) and in imatinib mesylate-resistant human leukemia cells (K562-R) in the presence and absence of imatinib mesylate. We identified 118 differentially regulated proteins in these two leukemia cell-lines, with and without a $1\;{\mu}M$ imatinib mesylate challenge. Nine proteins of unknown function were discovered. This is the first comprehensive report regarding differential protein expression in imatinib mesylate-treated CML cells.