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Yangsoo Jang,조봉준,Eun Kyoung Im,권준혜,이경혜,신혜진,Jaewon Oh,강석민,정지형 한국분자세포생물학회 2005 Molecules and cells Vol.20 No.3
Lysophosphatidylcholine (lysoPC) induces vascular smooth muscle cell (VSMC) proliferation and migration, which has been proposed to initiate the intimal thickening in coronary atherosclerotic lesions. Berberine is an alkaloid in Berberis aquifolium and many other plants. Recently, it has been shown to have beneficial effects on the cardiovascular system, such as anti-hyperglycemic and cholesterol-lowering activity. In this study, we investigated its effects on lysoPCinduced VSMC proliferation and migration. Berberine inhibited lysoPC-induced DNA synthesis and cell proliferation in VSMCs, as well as migration of the lysoPC-stimulated VSMCs. It also inhibited the activation of extracellular signal-regulated kinases (ERKs) and reduced transcription factor AP-1 activity and the lysoPC-induced increases in intracellular reactive oxygen species (ROS). These results indicate that the inhibitory effects of berberine on lysoPC-stimulated VSMC proliferation and migration are attributable to inhibition of ROS generation and hence of activation of the ERK1/2 pathway. This suggests that berberine has potential in the prevention of atherosclerosis and restenosis.
Jang, Yangsoo,Lee, Jong Ho,Chae, Jey Sook,Kim, Oh Yoen,Koh, Soo Jeong,Kim, Ji Young,Cho, Hongkeun,Lee, Jong Eun,Ordovas, Jose M Oxford University Press 2005 The American journal of clinical nutrition Vol.82 No.4
<P>BACKGROUND: The adiponectin gene is known to modulate adiponectin concentrations and diabetes mellitus development. OBJECTIVE: We assessed whether adiponectin gene variants contribute to circulating adiponectin, insulin resistance (IR), or cardiovascular disease risk factors. DESIGN: Nondiabetic subjects [n = 902; x +/- SE age: 42.5 +/- 0.53 y; body mass index (BMI; in kg/m2): 24.7 +/- 0.11] were genotyped for 2 single-nucleotide polymorphisms (SNPs), 45T-->G and 276G-->T. RESULTS: After adjustment for age, sex, and BMI, subjects with the G allele for the SNP 276 had significantly higher concentrations of triacylglycerol and small dense LDL (sdLDL) and smaller LDL particle size than did T/T subjects. G/G subjects at SNP 276 had significantly lower plasma adiponectin and higher homeostasis model assessment (HOMA) of IR and urinary prostaglandin F2alpha than did T/T subjects. In the SNP 45-276 haplotype test, we also observed that subjects with the X/X haplotype had significantly higher plasma adiponectin after adjustment than did TG/TG or TG/X haplotype subjects. In the highest BMI group (BMI > or = 26), T/T subjects had lower HOMA-IR (P = 0.011) and higher plasma adiponectin (P = 0.026) at SNP 276 than did G/G or G/T subjects. These patterns were also seen for adiponectin in haplotype groups. However, no significant genotype effect for SNP 45T-->G was observed. CONCLUSIONS: The 276G-->T polymorphism of the adiponectin gene modulates circulating adiponectin and IR, particularly in obese states. G allele carriers also have higher oxidative stress, higher sdLDL concentrations, and smaller LDL particle size. Therefore, the presence of the G allele in the adiponectin gene at SNP 276 could be a significant contributor to higher cardiovascular disease risk in Koreans, independent of common environmental factors.</P>
Thiamine Attenuates Hypoxia-induced Cell Death in Cultured Neonatal Rat Cardiomyocytes
Yangsoo Jang 한국분자세포생물학회 2004 Molecules and cells Vol.18 No.2
Previous studies have demonstrated that thiamine (vitamin B1) has a cytoprotective effect against ischemic damage to the heart, and that heat shock protein 70 (Hsp70) is capable of protecting cardiac cells from lethal ischemia/hypoxia. We show here that thiamine has a cytoprotective effect on cultured neonatal rat cardiomyocytes under hypoxic insult, and also protects the cardiomyocytes against hypoxia-induced apoptosis; caspase-3 activation, PARP cleavage and DNA fragmentation are all inhibited. Moreover, it increases the level of Hsp70 protein in the cardiomyocytes even under prolonged hypoxic stress and its effects on hypoxia- induced cardiac cell death are antagonized by an Hsp70 inhibitor. These results suggest that the cytoprotective effect of thiamine in cardiomyocytes under hypoxic stress is due to its ability to induce Hsp70.
Jang, Yangsoo,Chae, Jey Sook,Kim, Oh Yoen,Park, Hey Jun,Kim, Ji Young,Paik, Jean Kyung,Lee, Sang-Hyun,Lee, Jong Ho Elsevier 2010 Atherosclerosis Vol.211 No.2
<P><B>Abstract</B></P><P><B>Objective</B></P><P>We aimed to determine the influence of apolipoprotein A5 gene (<I>APOA5</I>)-1131<I>T</I>><I>C</I> single nucleotide polymorphism on the effects of dietary intervention and regular exercise (DIRE) targeting ApoA5 and triglyceride (TG) concentrations.</P><P><B>Methods</B></P><P>Hypertriglyceridemia patients (TG, 150–500mg/dL, <I>n</I>=283) undertook a 12-week DIRE (replacing 1/3 of refined rice in their diets with legumes, increasing vegetable intake, and regular walking).</P><P><B>Results</B></P><P>Pre-treatment, no genotype-related differences were detected in ApoA5, TG, or HDL cholesterol levels; however, post-treatment, subjects homozygous (<I>T</I>/<I>T</I>) for the <I>T</I> allele had lower serum TG (<I>P</I>=0.009) and higher HDL cholesterol (<I>P</I>=0.036) than other subjects. In <I>T</I>/<I>T</I> subjects, after adjustments for age, sex and weight changes (<I>r</I>1) or initial TG levels (<I>r</I>2), changes in ApoA5 levels negatively correlated with TG changes (<I>r</I>1=−0.29, <I>P</I>=0.05, <I>r</I>2=−0.28, <I>P</I><0.1) and positively correlated with changes in HDL cholesterol (<I>r</I>1=0.30, <I>P</I><0.05, <I>r</I>2=0.32, <I>P</I><0.05) and free fatty acid (<I>r</I>1=0.38, <I>P</I><0.01, <I>r</I>2=0.40, <I>P</I><0.01). In those with moderate hypertriglyceridemia (TG, 200–500mg/dL, <I>n</I>=130), <I>APOA5</I>-1131<I>T</I>/<I>T</I> carriers achieved significantly lower TG (<I>P</I>=0.007) and higher HDL cholesterol (<I>P</I><0.001) than −1131<I>C</I> allele carriers. Additionally, statistically significant interactions between the −1131<I>T</I>><I>C</I> and the compliance of DIRE were found for the change in TG (<I>P</I>=0.002) and HDL cholesterol (<I>P</I>=0.039). In good compliance group, <I>T</I>/<I>T</I> subjects showed greater reduction of TG and higher increase of HDL cholesterol than other subjects. On the other hand, non-good compliance group had no significant improvement in these variables.</P><P><B>Conclusions</B></P><P><I>APOA5</I>-1131<I>T</I>/<I>T</I> carriers may benefit more from the DIRE than <I>C</I> allele carriers. These effects were remarkable in patients with moderate hypertriglyceridemia and the individuals with good compliance.</P>
이경혜,정지형,Yangsoo Jang 생화학분자생물학회 2010 Experimental and molecular medicine Vol.42 No.10
Heat shock protein 90 (HSP90), one of the most abundant proteins in the cardiac cells is essential for cell survival. Previous studies have shown that angiotensin II induces cardiac cell hypertrophy. However,the role of HSP90 in the angiotensin II-induced cardiac hypertrophy is unclear. In this study, we showed that HSP90 regulated angiotensin II-induced hypertrophy via maintenance of the IκB kinase (IKK) complex stability in cardiac cells. An HSP90 inhibitor, geldanamycin (GA), significantly suppressed angiotensin II-induced [3H]leucine incorporation and atrial natriuretic factor expression in cardiac cells. GA also inhibited the NF-κB activation induced by angiotensin II. Importantly,treatment with GA caused a degradation of IKKα/β; on the other hand, a proteasome-specific inhibitor restored the level of IKKα/β. We also found that GA prevented HSP90-IKKs complex induced by angiotensin II in cardiac cells. The small interfering RNA (siRNA)-mediated knockdown of HSP90 expression significantly inhibited angiotensin II-induced cell hypertrophy and NF-κB activation. These results suggest that angiotensin II-induced cardiac hypertrophy requires HSP90 that regulates the stability and complex of IKK.