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Cho Rong Han(한초롱),Ji Young Lee(이지영),Dongki Kim(김동기),Hyo Young Kim(김효영),Se Jin Kim(김세진),Seokjoon Jang(장석준),Yoon Hee Kim(김윤희),Do Youn Jun(전도연),Young Ho Kim(김영호) 한국생명과학회 2013 생명과학회지 Vol.23 No.10
17α-estradiol (17α-E₂)의 에폽토시스 유도활성에 미치는 종양억제단백질 p53의 조절효과를 조사하고자, 17α-E₂에 의해 유도되는 에폽토시스 현상들을 인체 대장암 세포주 유래 클론인 HCT116 (p53+/+) 및 HCT116 (p53-/-) 세포에서 비교하였다. HCT116 (p53+/+) 및 HCT116 (p53-/-) 세포를 17α-E₂ (2.5~10 μM)로 처리하거나 혹은 HCT116 (p53+/+) 및 HCT116 (p53-/-) 세포를 10 μM 17α-E₂로 시간 별로 처리한 결과, HCT116 (p53+/+)에 있어서는 세포독성과 에폽토시스-관련 sub-G₁ peak의 비율은 처리농도와 시간에 의존적으로 나타났다. 그러나 HCT116 (p53-/-) 세포의 경우는 이러한 현상이 미약하게 나타났다. 17α-E₂에 의해 유도되는 비정상적 유사분열방추사 형성, 중기판 염색체 배열의 미완성, 이에 따른 유사분열정지(G₂/M arrest) 등의 현상은 HCT116 (p53+/+) 및 HCT116 (p53-/-) 세포에서 유사한 수준으로 나타났다. 이에 반해, 17α-E₂에 의해 유도되는 Bak과 Bax의 활성화, 미토콘드리아의 막전위 상실(Δψm loss), 그리고 PARP 분해 등의 현상은 HCT116 (p53-/-) 세포에 비해 HCT116 (p53+/+) 세포에서 훨씬 높은 수준으로 확인되었다. 아울러 17α-E₂로 처리된 HCT116 (p53+/+) 세포에서 확인되는 p53 (Ser-15)의 인산화 및 p53 수준의 증가와 일치하여, 세포 내의 p21및 Bax 수준도 현저히 증가하였다. 이때 17α-E2로 처리된 HCT116 (p53-/-) 세포에서는 p21 및 Bax의 발현수준이 매우 낮았다. 한편, 에폽토시스 억제단백질인 Bcl-2 단백질수준은 HCT116 (p53-/-) 세포에 비해 HCT116 (p53+/+) 세포에서 다소 낮았으나, 이러한 Bcl-2 단백질 수준은 17α-E₂ 처리 후에도 크게 변화하지 않는 것으로 나타났다. 이러한 결과들은 17α-E₂ 처리에 의해 유도되는 에폽토시스 유도 경로의 구성원들의 변화, 즉 비정상적 유사분열방추사 형성 및 이에 따른 유사분열정지(G2/M arrest), 뒤이은 Bak 및 Bax의 활성화, 미토콘드리아의 막전위 상실, 그리고 이에 수반되는 caspase cascade 활성화 및 PARP 분해로 진행되는 에폽토시스 현상들 중에서, Bak 및 Bax의 활성화 단계가 종양억제단백질 p53의 에폽토시스 증진 활성에 의해 양성적으로 조절되는 작용 타켓임을 보여준다. The regulatory effect of the tumor-suppressor protein p53 on the apoptogenic activity of 17α-estradiol (17α-E₂) was compared between HCT116 (p53+/+) and HCT116 (p53-/-) cells. When the HCT116 (p53+/+) and HCT116 (p53-/-) cells were treated with 2.5~10 μM 17α-E₂ for 48 h or with 10 μM for various time periods, cytotoxicity and an apoptotic sub-G₁ peak were induced in the HCT116 (p53+/+) cells in a dose- and time-dependent manner. However, the HCT116 (p53-/-) cells were much less sensitive to the apoptotic effect of 17α-E₂. Although 17α-E₂ induced aberrant mitotic spindle organization and incomplete chromosome congregation at the equatorial plate, G₂/M arrest was induced to a similar extent in both cell types. In addition, 17α-E₂-induced activation of Bak and Bax, Δψm loss, and PARP degradation were more dominant in the HCT116 (p53+/+) than in the HCT116 (p53-/-) cells. In accordance with enhancement of p53 phosphorylation (Ser-15) and p53 levels, p21 and Bax levels were elevated in the HCT116 (p53+/+) cells treated with 17α-E₂. The HCT116 (p53-/-) cells exhibited barely or undetectable levels of p21 and Bax, regardless of 17α-E₂ treatment. On the other hand, although the level of Bcl-2 was slightly lower in the HCT116 (p53+/+) than in the HCT116 (p53-/-) cells, it remained relatively constant after the 17α-E₂ treatment. Together, these results show that among the components of the 17α-E₂-induced apoptotic-signaling pathway, which proceeds through mitotic spindle defects causing mitotic arrest, subsequent activation of Bak and Bax and the mitochondria-dependent caspase cascade, leading to PARP degradation, 17α-E₂-induced activation of Bak and Bax is the upstream target of proapoptotic action of p53.
전도연,Cho Rong Han,Ji Young Lee,Wan Park,최명숙,Mi Hee Woo,김영호 한국식품영양과학회 2011 Journal of medicinal food Vol.14 No.5
To examine anti-adipogenic activity of 2-carbomethoxy-2,3-epoxy-3-prenyl-1,4-naphthoquinone (CMEP-NQ) isolated from the roots of Rubia cordifolia L., its effects on cell viability, apoptosis, and adipogenesis in 3T3-L1 preadipocytes were investigated. The inhibitory effect of CMEP-NQ on cell viability was more significant in differentiated mature adipocytes than in 3T3-L1 preadipocytes. In 3T3-L1 cells, the cytotoxicity of CMEP-NQ (20–40 μM) was accompanied by apoptotic events such as mitochondrial membrane potential loss, caspase-3 activation, poly(ADP-ribose) polymerase degradation, and terminal deoxynucleotidyl transferase-meidated dUTP nick-end labeling–positive apoptotic DNA fragmentation. Although the presence of 10 μM CMEP-NQ during induced adipocytic differentiation of 3T3-L1 cells for 6 days failed to influence the cell viability, it did reduce the differentiation-associated accumulation of intracellular lipid by approximately 48.5%. A similar level of inhibition was observed when 10 μM CMEP-NQ was present during the early stage (Days 0–2) of the differentiation period. At the same time, the expressions of CCAAT/enhancer binding protein-α, peroxisome proliferator-activated receptor γ1, peroxisome proliferator-activated receptor γ2, and adiponectin were down-regulated. However, the presence of 10 μM CMEP-NQ during either the middle (Days 2–4) or late (Days 4–6) stage of the differentiation period caused the inhibition to a lesser extent. These results indicated that CMEP-NQ at high concentrations (20–40 μM) exerted cytotoxicity via inducing apoptosis, whereas CMEP-NQ at a low concentration (10 μM) suppressed adipocytic differentiation without exerting cytotoxicity in 3T3-L1 preadipocytes.
Interpretation of Stress Crack Resistance of Damaged Geomembranes
전한용(Han-Yong Jeon),김윤진(Yoon-Jin Kim),김주희(Ju-Hee Kim),김초롱(Cho-Rong Kim) 한국토목섬유학회 2009 한국토목섬유학회 학술발표회 Vol.2009 No.4
Smooth 타입과 textured 타입의 HDPE 지오멤브레인 시편을 각각 40, 60℃ 조건하에서 NCTL 실험을 시행하였다. 실험결과 notch 처리를 한 시편은 탁월한 산화저항성을 나타내었다. HDPE 지오 멤브레인은 산성과 알칼리성 조건하에서 우수한 stress crack 저항과 우수한 화학저항성을 나타내었다. 그렇지만 온도와 하중의 증가에 따라 stress crack 저항성은 감소하였다. SEM 사진을 통하여 인장강도 시험 후 시편의 표면에 큰 변화가 있는 것을 볼 수 있었다. 온도가 40℃ 미만일 때 Smooth와 textured 타입, notched 처리를 한 시료와 하지 않은 시료의 기계적 성능의 변화는 발견되지 않았고 60 및 80℃에서는 큰 차이가 나타났다.
Defective erythropoiesis caused by mutations of the thyroid hormone receptor α gene
Park, Sunmi,Han, Cho Rong,Park, Jeong Won,Zhao, Li,Zhu, Xuguang,Willingham, Mark,Bodine, David M.,Cheng, Sheue-yann,Grimes, H. Leighton Public Library of Science 2017 PLoS genetics Vol.13 No.9
<▼1><P>Patients with mutations of the <I>THRA</I> gene exhibit classical features of hypothyroidism, including erythroid disorders. We previously created a mutant mouse expressing a mutated TRα1 (denoted as PV; <I>Thra1</I><SUP>PV/+</SUP> mouse) that faithfully reproduces the classical hypothyroidism seen in patients. Using <I>Thra1</I><SUP>PV/+</SUP> mice, we explored how the TRα1PV mutant acted to cause abnormalities in erythropoiesis. <I>Thra1</I><SUP>PV/+</SUP> mice exhibited abnormal red blood cell indices similarly as reported for patients. The total bone marrow cells and erythrocytic progenitors were markedly reduced in the bone marrow of <I>Thra1</I><SUP>PV/+</SUP> mice. <I>In vitro</I> terminal differentiation assays showed a significant reduction of mature erythrocytes in <I>Thra1</I><SUP>PV/+</SUP> mice. In wild-type mice, the clonogenic potential of progenitors in the erythrocytic lineage was stimulated by thyroid hormone (T3), suggesting that T3 could directly accelerate the differentiation of progenitors to mature erythrocytes. Analysis of gene expression profiles showed that the key regulator of erythropoiesis, the <I>Gata-1</I> gene, and its regulated genes, such as the <I>Klf1</I>, <I>β-globin</I>, <I>dematin</I> genes, <I>CAII</I>, <I>band3 and eALAS</I> genes, involved in the maturation of erythrocytes, was decreased in the bone marrow cells of <I>Thra1</I><SUP>PV/+</SUP> mice. We further elucidated that the <I>Gata-1</I> gene was a T3-directly regulated gene and that TRα1PV could impair erythropoiesis via repression of the <I>Gata-1</I> gene and its regulated genes. These results provide new insights into how TRα1 mutants acted to cause erythroid abnormalities in patients with mutations of the <I>THRA</I> gene. Importantly, the <I>Thra1</I><SUP>PV/+</SUP> mouse could serve as a preclinical mouse model to identify novel molecular targets for treatment of erythroid disorders.</P></▼1><▼2><P><B>Author summary</B></P><P>Patients with mutations of the <I>THRA</I> gene exhibit erythroid disorders. The molecular pathogenesis underlying erythroid abnormalities is poorly understood. In <I>Thra1</I><SUP>PV/+</SUP> mice expressing a dominant negative mutant TRα1PV, we found abnormal red blood cell indices similar to patients. Total bone marrow cells, the clonogenic potential of erythrocytic progenitors, and terminal differentiation of erythrocytes were markedly decreased in <I>Thra1</I><SUP>PV/+</SUP> mice. We elucidated that <I>Gata-1</I>, a key erythroid gene, was directly positively regulated by TRα1. The erythroid defects in <I>Thra1</I><SUP>PV/+</SUP> mice were due, at least partly, to the TRα1PV-mediated suppression of the <I>Gata-1</I> gene and its down-stream target genes. Over-expression of <I>Gata-1</I> rescued impaired terminal differentiation. Our studies elucidated molecular mechanisms by which TRα1 mutants caused erythroid disorders in patients. The present study suggests that therapies aimed at GATA1 could be tested as a potential target in treating erythroid abnormalities in patients.</P></▼2>