Hyo Shin Kim
Chungnam National University
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Featured researches published by Hyo Shin Kim.
Circulation Research | 2009
Hwan Myung Lee; Byeong Hwa Jeon; Kyung-Jong Won; Chang-Kwon Lee; Tae-Kyu Park; Wahn Soo Choi; Young Min Bae; Hyo Shin Kim; Sang Ki Lee; Seung Hwa Park; Kaikobad Irani; Bokyung Kim
The role of apurinic/apyrimidinic endonuclease-1/redox factor-1 (Ref-1) in vascular smooth muscle cells has yet to be clearly elucidated. Therefore, we attempted to determine the roles of Ref-1 in the migration induced by platelet-derived growth factor (PDGF)-BB and in its signaling in rat aortic smooth muscle cells (RASMCs). Cellular migration, superoxide (O2−·) production, Rac-1 activity, and neointima formation were determined in cells transfected with adenoviruses encoding for Ref-1 (AdRef-1) and small interference RNA of Ref-1. Overexpression of Ref-1 induced by treatment with RASMCs coupled with AdRef-1 inhibited the migration induced by PDGF-BB. PDGF-BB also increased the phosphorylation of the PDGF&bgr; receptor, spleen tyrosine kinase (Syk), mitogen-activated protein kinase, and heat shock protein 27, but these increases were significantly inhibited by AdRef-1 treatment. PDGF-BB increased O2−· production and Rac-1 activity, and these were diminished in cells transfected with AdRef-1. In contrast, RASMC migration, phosphorylation of Syk and O2−· production in response to PDGF-BB were increased by the knock down of Ref-1 with small interference RNA. The phosphorylation of PDGF&bgr; receptor in response to PDGF-BB was inhibited completely by the Syk inhibitor and was partly attenuated by a NADPH oxidase inhibitor. PDGF-BB increased the sprout outgrowth of the aortic ring ex vivo, which was inhibited in the AdRef-1–infected RASMCs as compared with the controls. Balloon injury–induced neointimal formation was significantly attenuated by the gene transfer of AdRef-1. These results indicate that Ref-1 inhibits the PDGF-mediated migration signal via the inhibition of reactive oxygen species–mediated Syk activity in RASMCs.
Anesthesiology | 2009
Hee Kyoung Joo; Sae Cheol Oh; Eun Jung Cho; Kyoung Sook Park; Ji Young Lee; Eun Ji Lee; Sang Ki Lee; Hyo Shin Kim; Jin Bong Park; Byeong Hwa Jeon
Background:Midazolam is widely used as an intravenous sedative. However, the role of midazolam on vascular endothelial activation is still unknown. The present study explores the action of midazolam on endothelial activation and its role to peripheral benzodiazepine receptor (PBR) in cultured human umbilical vein endothelial cells. Methods:Intracellular localization of PBR in human umbilical vein endothelial cells was visualized with immunofluorescent staining. Monocyte adhesion and vascular cell adhesion molecule-1 expression were measured with monocyte adhesion assay and Western blot analysis. Involvement of PBR was assessed by using specific antagonists and small interfering RNA against PBR. Results:PBR was localized in the mitochondria of human umbilical vein endothelial cells. Midazolam significantly inhibited tumor necrosis factor-&agr;–induced vascular cell adhesion molecule-1 and monocyte adhesion in a dose-dependent manner (1–30 &mgr;M). The midazolam-mediated suppression on the tumor necrosis factor-&agr;–induced vascular cell adhesion molecule-1 expression and monocyte adhesion were inhibited by the pretreatment of PK11195 and not inhibited by the flumazenil. Transfection of small interfering RNA for PBR decreased the expression of PBR (18 kDa) in human umbilical vein endothelial cells. Midazolam-mediated suppression on the tumor necrosis factor-&agr;–induced vascular cell adhesion molecule-1 expression was abrogated by the transfection of small interfering RNA for PBR. Conclusion:These results suggest that midazolam has an inhibitory action on the endothelial activation and that its action is related to the activation of peripheral benzodiazepine receptor localized in mitochondria of the endothelial cells.
FEBS Letters | 2008
Sang Ki Lee; Hyo Shin Kim; Yun Jeong Song; Hee Kyoung Joo; Ji Young Lee; Kwon Ho Lee; Eun Jung Cho; Chung-Hyun Cho; Jin Bong Park; Byeong Hwa Jeon
To examine the role of p66shc in endothelial dysfunction, we investigated the endothelium‐dependent relaxation, protein expression and superoxide production in abdominal aortic coarctation rats. Endothelium‐dependent relaxation to acetylcholine was impaired only in the aortic segments above the aortic coarctation (35.0±7.1% vs. 86.6 ± 6.0% for sham control at 1 μM Ach). The aortic segments exposed to increased blood pressure showed a decreased phosphorylation of endothelial nitric oxide synthase, an increased phosphorylation of p66shc, and an increased superoxide production. Angiotensin II elicited a significantly increased phosphorylation of p66shc in the endothelial cells. Taken together, these findings suggest that the increased phosphorylation of p66shc is one of the important mediators in the impaired endothelium‐dependent relaxation of aortic coarctation rats.
Biochemical and Biophysical Research Communications | 2013
Sunga Choi; Yu Ran Lee; Myoung Soo Park; Hee Kyoung Joo; Eun Jung Cho; Hyo Shin Kim; Cuk Seong Kim; Jin Bong Park; Kaikobad Irani; Byeong Hwa Jeon
Apurinic/apyrimidinic endonuclease 1/Redox factor-1 (APE1/Ref-1) can be acetylated via post-translational modification. We investigated the effect of an inhibitor of histone deacetylases on the extracellular release of APE1/Ref-1 in HEK293 cells. Trichostatin A (TSA), an inhibitor of histone deacetylases, induced APE1/Ref-1 secretion without changing cell viability. In a fluorescence quantitative assay, the secreted APE1/Ref-1 was estimated to be about 10 ng/mL in response to TSA (1 μM). However, TSA did not induce the secretion of lysine-mutated APE1/Ref-1 (K6R/K7R). TSA also caused nuclear to cytoplasmic translocation of APE1/Ref-1. Taken together, these findings suggest that APE1/Ref-1 is a protein whose secretion is governed by lysine acetylation.
Biochemical and Biophysical Research Communications | 2008
Yun Jeong Song; Ji Young Lee; Hee Kyoung Joo; Hyo Shin Kim; Sang Ki Lee; Kwon Ho Lee; Chung-Hyun Cho; Jin Bong Park; Byeong Hwa Jeon
Apurinic/apyrimidinic endonuclease 1/redox factor-1 (APE1/ref-1) is a multifunctional protein involved both in DNA base excision repair and redox regulation. In this study we evaluated the protective role of Tat-mediated APE1/ref-1 transduction on the tumor necrosis factor (TNF)-alpha-activated endothelial activation in cultured human umbilical vein endothelial cells. To construct Tat-APE1/ref-1 fusion protein, human full length of APE1/ref-1 was fused with Tat-protein transduction domain. Purified Tat-APE1/ref-1 fusion protein efficiently transduced cultured endothelial cells in a dose-dependent manner and reached maximum expression at 1h after incubation. Transduced Tat-APE1/ref-1 showed inhibitory activity on the TNF-alpha-induced monocyte adhesion and vascular cell adhesion molecule-1 expression in cultured endothelial cells. These results suggest Tat-APE1/ref-1 might be useful to reduce vascular endothelial activation or vascular inflammatory disorders.
Food and Environmental Virology | 2010
Sang-Hun Park; Eun-Jeung Kim; T. H. Yun; Jae-In Lee; Chang-Kyu Kim; Y. H. Seo; Seah Oh; Sungmin Choi; Moo-Sang Kim; G.-Y. Han; Mi-Sun Kim; H. S. Jeong; Doo-Sung Cheon; Hyo Shin Kim
Waterborne outbreaks of enteric viruses are a major public health concern. The present study has been carried out to assess the presence of enteric viruses responsible for human acute gastroenteritis (AGE) in groundwater intended for drinking and produce washing. In total, 62 samples from groundwater for drinking and produce washing collected from Dec 2007 to Dec 2008 in Seoul were tested for enteric viruses using conventional RT–PCR, ELISA, and real-time RT–PCR. Our results showed that enteric viruses were detected in 7 (8.8%) groundwater samples. Rotaviruses were detected in 3 (4.8%) of the samples by ELISA; human adenoviruses were detected in 2 (3.2%) of the samples by ELISA; and nested RT–PCR detected noroviruses in 2 (3.2%) of the samples. In one of the groundwater sample, the norovirus RNA was detected by conventional RT–PCR which was confirmed positive by real-time RT–PCR. Additionally, real-time RT–PCR successfully detected norovirus RNA in five out of 62 water samples (8.1%). The data demonstrate that real-time RT–PCR will be useful as a rapid and sensitive method for detecting norovirus in water samples. Phylogenetic analysis revealed that the noroviruses detected in two of the groundwater samples belonged to GII-4. These studies can provide important information for the prevalence of enteric viruses in Korean groundwater.
Biochemical and Biophysical Research Communications | 2009
Sang Ki Lee; Cuk Seong Kim; Hyo Shin Kim; Eun Jung Cho; Hee Kyoung Joo; Ji Young Lee; Eun Ji Lee; Jin Bong Park; Byeong Hwa Jeon
We investigated the role that endothelial nitric oxide synthase plays in post-exercise hypotension in spontaneously hypertensive rats. To accomplish this, rats were subjected to a single bout of dynamic exercise on a treadmill at 15 m/min for 20 min. L-nitroarginine methyl ester (L-NAME, 40 mg/kg, i.p.) significantly inhibited post-exercise hypotension (25+/-11 and 5+/-3 mm Hg, respectively; P<0.05). In addition, the superoxide anion generation was decreased, while the plasma nitrite production and serine phosphorylation of endothelial nitric oxide synthase were significantly elevated in spontaneously hypertensive rats at 30 min after the termination of exercise. Taken together, these data demonstrate that the increased phosphorylation of endothelial nitric oxide synthase plays a crucial role in the reduction of arterial pressure following a single bout of dynamic exercise in spontaneously hypertensive rats.
Journal of Ginseng Research | 2008
Hee Kyoung Joo; Sang Ki Lee; Hyo Shin Kim; Yun Jeong Song; Gun Kang; Jin Bong Park; Kwon Ho Lee; Eun Jung Cho; Jae-Hwan Lee; In-Whan Seong; Se Hoon Kim; Chung-Hyun Cho; Byeong Hwa Jeon
Vascular inflammation is an important step in the development of cardiovascular disorder. Since it has not been known whether Korean red ginseng has a role to play on the vascular inflammation, we investigated the effects of Korean red ginseng extract (KRGE) on monocyte adhesion and its underlying signaling mechanism. Monocyte adhesion assay and Western blot were conducted on the human umbilical vein endothelial cells to study monocyte adhesion and the expression of adhesion molecules. Intracellular calcium was measured with Fura-2 fluorescent staining, and superoxide production was measured with lucigenin chemiluminescence in the endothelial cells. KRGE inhibits tumor necrosis factor (TNF)-alpha-induced monocyte adhesion on the endothelial cells at the range of 0.03~1 ㎎/㎖. TNF-alpha-induced vascular cell adhesion molecule-1 and intercellular cell adhesion molecule-1 expression were inhibited by the pretreatment of KRGE in the endothelial cells. KRGE also inhibits TNF-alpha-induced intracellular calcium and the superoxide production in the endothelial cells. This study first demonstrated that KRGE inhibits TNF-alpha-induced monocyte adhesion by inhibiting the adhesion molecule expression, intracellular calcium and superoxide production in the endothelial cells. Therefore, the anti-inflammatory function of KRGE may be contributed to protecting the endothelial dysfunction in the vascular inflammatory disorders.
The Korean Journal of Physiology and Pharmacology | 2009
Kwon Ho Lee; Sang Ki Lee; Hyo Shin Kim; Eun Jung Cho; Hee Kyoung Joo; Eun Ji Lee; Ji Young Lee; Myoung Soo Park; Seok Jong Chang; Chung-Hyun Cho; Jin Bong Park; Byeong Hwa Jeon
The role of apurinic/apyrimidinic endonuclease1/redox factor-1 (Ref-1) on the lead (Pb)-induced cellular response was investigated in the cultured endothelial cells. Pb caused progressive cellular death in endothelial cells, which occurred in a concentration- and time-dependent manner. However, Ref-1 overexpression with AdRef-1 significantly inhibited Pb-induced cell death in the endothelial cells. Also the overexpression of Ref-1 significantly suppressed Pb-induced superoxide and hydrogen peroxide elevation in the endothelial cells. Pb exposure induced the downregulation of catalase, it was inhibited by the Ref-1 overexpression in the endothelial cells. Taken together, our data suggests that the overexpression of Ref-1 inhibited Pb-induced cell death via the upregulation of catalase in the cultured endothelial cells.
European Journal of Clinical Microbiology & Infectious Diseases | 2009
Sang-Hun Park; Eun-Jeung Kim; J.-H. Lee; Sungmin Choi; Moo-Sang Kim; S.-S. Jung; G.-Y. Han; H.-S. Yun; D.-S. Chun; S.-S. Oh; Hyo Shin Kim
Hepatitis A virus (HAV) is a major public health problem throughout the world. As a result of declining HAV endemic in Korea, an increasing number of children and adolescents have become susceptible to HAV infection. HAV is related with sanitation conditions of the environment and is transmitted via the fecal–oral route, either through person-to-person contact or by contaminated water and food. The present study has been carried out to determine the phylogenetic analysis and circulating patterns of HAV strains detected from hospitalized patients with acute gastroenteritis (AGE) in the Seoul region of Korea. In total, 2,782 stool specimens from hospitalized patients with AGE collected in October 2006 to September 2007 in Seoul were tested for HAV. A pair comparison of the nucleic acid sequence of a 159-bp base region at the putative VP1/2A junction of 85 Seoul isolates revealed that the most common HAV strain circulating in the region during 2006–2007 was subgenotype IA. HAV phylogenetic studies can provide important information on the genetic characteristics of HAV from AGE patients who may subsequently become the source of infection in Korea.