• Development and Reproduction
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• v.15 no.4
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• pp.273-279
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• 2011

Epigenetic regulation is a phenomenon that changes the gene function without changing the underlying DNA sequences. Epigenetic status of chromosome is regulated by mechanisms such as histone modification, DNA modification, and RNAi silencing. In this review, we focused on histone methylation for epigenetic regulation in ES cells. Two antagonizing multiprotein complexes regulate methylation of histones to guide expression of genes in ES cells. The Polycomb repressive complex 2 (PRC2), including EED, EZH2, and SUZ12 as core factors, contributes to gene repression by increasing trimethylation of H3K27 (H3K27me3). In contrast, the Trithorax group (TrxG) complex including MLL is related to gene activation by making H3K4me3. PRC2 and TrxG accompany a variety of accessory proteins. Most prominent feature of epigenetic regulation in ES cells is a bivalent state in which H3K27me3 and H3K4me3 appear simultaneously. Concerted regulation of PRC2, TrxG complex, and H3K4- or H3K27-specific demethylases activate expression of pluripotency-related genes and suppress development-related genes in ES cells. Modified balance of the regulators also enables ES cells to efficiently differentiate to a variety of cells upon differentiating signals. More detailed insights on the epigenetic regulators and their action will lead us to better understanding and use of ES cells for future application.

• Journal of Yeungnam Medical Science
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• v.3 no.1
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• pp.313-318
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• 1986

Primary aldosteronism is a disease that the stimulus for the excessive aldosterone production resides within the adrenal gland. It was first described by conn in 1955. And many cases were reported by physicians at present in the world. But it is relatively rare in Korea, probably due to lack of attension and medical facilities. Only about 13 cases have been reported at present. The clinical, biochemical features in 1 case of primary aldosteranism caused by adrenal hyperplasia that was diagnosed at Yeungnam University Hospital was observed and the following result were obtained. 1. Clinical feature: The present case was 27-year-old woman who was admitted due to general weakness and easy fatigability. The above mensioned chief complaints occurred 8 months prior to admission when she delivered of second baby by cesarian section. Symptoms such as above chief complaints, intermittent muscle paralysis and cramping were noticed. Trousseau's sign was also present. The average blood pressure ranged from 170/90 to 200/120. 2. Biochemical abnormalities: Severe hypokalemia lower than 2.5 mEq/L was presented and 24 hours urine potassium showed markedly increased urinary loss.(228 mEq/day). Plasma renin activity was decreased under normal range with furosemide administration.(Basal renin; 0.01ng/ml/hr, stimulated renin 0.12ng/ml/hr). Saline suppression test revealed markedly elevated levels of aldosterone higher than normal range. (Basal aldosterone; 320.68pg/ml stimulated aldosterone; 451.86pg/ml). And posture test showed decreased plasma renin activity and increased plasma aldosterone level. - PRA(ng/ml/hr)=Bsal: 0.05(0.15~2.33), Stimulated: 0.22(1.31~3.95) - Aldosterone(pg/ml)=Bsal: 242.77(10~160), Stimulated: 432.09(40~310) 3. Adrenal CT scan revealed no abnormal findings. 4. Treatment and course: Spironolactone was given at OPD with regular follow-up. Her blood pressure ranged from 150/90 to 160/100 and symptoms were improved. The effect of treatment was satisfactory and further follow up would be performed.

• BMB Reports
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• v.52 no.10
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• pp.595-600
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• 2019

Cardiac fibrosis is a common feature in chronic hypertension patients with advanced heart failure, and endothelial-to-mesenchymal transition (EndMT) is known to promote Angiotensin II (Ang II)-mediated cardiac fibrosis. Previous studies have suggested a potential role for the transcription factor, ETS-1, in Ang II-mediated cardiac remodeling, however the mechanism are not well defined. In this study, we found that mice with endothelial Ets-1 deletion showed reduced cardiac fibrosis and hypertrophy following Ang II infusion. The reduced cardiac fibrosis was accompanied by decreased expression of fibrotic matrix genes, reduced EndMT with decreased Snail, Slug, Twist, and ZEB1 expression, as well as reduced cardiac hypertrophy and expression of hypertrophy-associated genes was observed. In vitro studies using cultured H5V cells further confirmed that ETS-1 knockdown inhibited $TGF-{\beta}1$-induced EndMT. This study revealed that deletion of endothelial Ets-1 attenuated Ang II-induced cardiac fibrosis via inhibition of EndMT, indicating an important ETS-1 function in mediating EndMT. Inhibition of ETS-1 could be a potential therapeutic strategy for treatment of heart failure secondary to chronic hypertension.