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Search Results: 1 - 10 of 20880 matches for " Bong-Seon Kim "
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Hedgehog Signaling Regulates the Survival of Gastric Cancer Cells by Regulating the Expression of Bcl-2
Myoung-Eun Han,Young-Suk Lee,Sun-Yong Baek,Bong-Seon Kim,Jae-Bong Kim,Sae-Ock Oh
International Journal of Molecular Sciences , 2009, DOI: 10.3390/ijms10073033
Abstract: Gastric cancer is the second most common cause of cancer deaths worldwide. The underlying molecular mechanisms of its carcinogenesis are relatively poorly characterized. Hedgehog (Hh) signaling, which is critical for development of various organs including the gastrointestinal tract, has been associated with gastric cancer. The present study was undertaken to reveal the underlying mechanism by which Hh signaling controls gastric cancer cell proliferation. Treatment of gastric cancer cells with cyclopamine, a specific inhibitor of Hh signaling pathway, reduced proliferation and induced apoptosis of gastric cancer cells. Cyclopamine treatment induced cytochrome c release from mitochondria and cleavage of caspase 9. Moreover, Bcl-2 expression was significantly reduced by cyclopamine treatment. These results suggest that Hh signaling regulates the survival of gastric cancer cells by regulating the expression of Bcl-2.
LAP2 Is Widely Overexpressed in Diverse Digestive Tract Cancers and Regulates Motility of Cancer Cells
Hyun-Jung Kim, Sun-Hwi Hwang, Myoung-Eun Han, Sungmin Baek, Hey-Eun Sim, Sik Yoon, Sun-Yong Baek, Bong-Seon Kim, Jeong-Hwan Kim, Seon-Young Kim, Sae-Ock Oh
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0039482
Abstract: Background Lamina-associated polypeptides 2 (LAP2) is a nuclear protein that connects the nuclear lamina with chromatin. Although its critical roles in genetic disorders and hematopoietic malignancies have been described, its expression and roles in digestive tract cancers have been poorly characterized. Methods To examine the expression of LAP2 in patient tissues, we performed immunohistochemistry and real-time PCR. To examine motility of cancer cells, we employed Boyden chamber, wound healing and Matrigel invasion assays. To reveal its roles in metastasis in vivo, we used a liver metastasis xenograft model. To investigate the underlying mechanism, a cDNA microarray was conducted. Results Immunohistochemistry in patient tissues showed widespread expression of LAP2 in diverse digestive tract cancers including stomach, pancreas, liver, and bile duct cancers. Real-time PCR confirmed that LAP2β is over-expressed in gastric cancer tissues. Knockdown of LAP2β did not affect proliferation of most digestive tract cancer cells except pancreatic cancer cells. However, knockdown of LAP2β decreased motility of all tested cancer cells. Moreover, overexpression of LAP2β increased motility of gastric and pancreatic cancer cells. In the liver metastasis xenograft model, LAP2β increased metastatic efficacy of gastric cancer cells and mortality in tested mice. cDNA microarrays showed the possibility that myristoylated alanine-rich C kinase substrate (MARCKS) and interleukin6 (IL6) may mediate LAP2β-regulated motility of cancer cells. Conclusions From the above results, we conclude that LAP2 is widely overexpressed in diverse digestive tract cancers and LAP2β regulates motility of cancer cells and suggest that LAP2β may have utility for diagnostics and therapeutics in digestive tract cancers.
Regulation of cerebrospinal fluid production by caffeine consumption
Myoung-Eun Han, Hak-Jin Kim, Young-Suk Lee, Dong-Hyun Kim, Joo-Taek Choi, Chul-Sik Pan, Sik Yoon, Sun-Yong Baek, Bong-Seon Kim, Jae-Bong Kim, Sae-Ock Oh
BMC Neuroscience , 2009, DOI: 10.1186/1471-2202-10-110
Abstract: In the present study we found that the long-term consumption of caffeine can induce ventriculomegaly; this was observed in 40% of the study rats. In the caffeine-treated rats with ventriculomegaly, there was increased production of CSF, associated with the increased expression of Na+, K+-ATPase and increased cerebral blood flow (CBF). In contrast to the chronic effects, acute treatment with caffeine decreased the production of CSF, suggesting 'effect inversion' associated with caffeine, which was mediated by increased expression of the A1 adenosine receptor, in the choroid plexus of rats chronically treated with caffeine. The involvement of the A1 adenosine receptor in the effect inversion of caffeine was further supported by the induction of ventriculomegaly and Na+, K+-ATPase, in A1 agonist-treated rats.The results of this study show that long-term consumption of caffeine can induce ventriculomegaly, which is mediated in part by increased production of CSF. Moreover, we also showed that adenosine receptor signaling can regulate the production of CSF by controlling the expression of Na+, K+-ATPase and CBF.Methylxanthine caffeine is present in many common beverages, and is widely consumed worldwide [1,4]. Caffeine consumption has been estimated to be 76 mg per person per day worldwide, as high as 238 mg per person per day in the United States and Canada, and more than 400 mg per person per day in Sweden and Finland [5,6]. Caffeine is absorbed rapidly after oral administration and distributed to various organs and tissues. In the liver, caffeine is metabolized to dimethyl- and monomethylxanthines, dimethyl and monomethyl uric acids, trimethyl- and dimethylallantoin, and uracil derivatives. Some metabolites of caffeine including 1,3-dimethylxanthine (theophylline) and 1,7-dimethylxanthine (paraxanthine) have pharmacological activity similar to caffeine [4]. The half-life of caffeine is ~5 hours in humans and ~1 hour in rats [4,7].The main mechanism of action of caffei
NESH Regulates Dendritic Spine Morphology and Synapse Formation
Jeomil Bae, Bong Hwan Sung, In Ha Cho, Seon-Myung Kim, Woo Keun Song
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0034677
Abstract: Background Dendritic spines are small membranous protrusions on the neuronal dendrites that receive synaptic input from axon terminals. Despite their importance for integrating the enormous information flow in the brain, the molecular mechanisms regulating spine morphogenesis are not well understood. NESH/Abi-3 is a member of the Abl interactor (Abi) protein family, and its overexpression is known to reduce cell motility and tumor metastasis. NESH is prominently expressed in the brain, but its function there remains unknown. Methodology/Principal Findings NESH was strongly expressed in the hippocampus and moderately expressed in the cerebral cortex, cerebellum and striatum, where it co-localized with the postsynaptic proteins PSD95, SPIN90 and F-actin in dendritic spines. Overexpression of NESH reduced numbers of mushroom-type spines and synapse density but increased thin, filopodia-like spines and had no effect on spine density. siRNA knockdown of NESH also reduced mushroom spine numbers and inhibited synapse formation but it increased spine density. The N-terminal region of NESH co-sedimented with filamentous actin (F-actin), which is an essential component of dendritic spines, suggesting this interaction is important for the maturation of dendritic spines. Conclusions/Significance NESH is a novel F-actin binding protein that likely plays important roles in the regulation of dendritic spine morphogenesis and synapse formation.
EGb761, a Ginkgo Biloba Extract, Is Effective Against Atherosclerosis In Vitro, and in a Rat Model of Type 2 Diabetes
Soo Lim, Ji Won Yoon, Seon Mee Kang, Sung Hee Choi, Bong Jun Cho, Min Kim, Ho Seon Park, Hyun Ju Cho, Hayley Shin, Young-Bum Kim, Hyo Soo Kim, Hak Chul Jang, Kyong Soo Park
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0020301
Abstract: Background EGb761, a standardized Ginkgo biloba extract, has antioxidant and antiplatelet aggregation and thus might protect against atherosclerosis. However, molecular and functional properties of EGb761 and its major subcomponents have not been well characterized. We investigated the effect of EGb761 and its major subcomponents (bilobalide, kaemferol, and quercetin) on preventing atherosclerosis in vitro, and in a rat model of type 2 diabetes. Methods and Results EGb761 (100 and 200 mg/kg) or normal saline (control) were administered to Otsuka Long-Evans Tokushima Fatty rats, an obese insulin-resistant rat model, for 6 weeks (from 3 weeks before to 3 weeks after carotid artery injury). Immunohistochemical staining was performed to investigate cell proliferation and apoptosis in the injured arteries. Cell migration, caspase-3 activity and DNA fragmentation, monocyte adhesion, and ICAM-1/VCAM-1 levels were explored in vitro. Treatment with EGb761 dose-dependently reduced intima-media ratio, proliferation of vascular smooth muscle cells (VSMCs) and induced greater apoptosis than the controls. Proliferation and migration of VSMCs in vitro were also decreased by the treatment of EGb761. Glucose homeostasis and circulating adiponectin levels were improved, and plasma hsCRP concentrations were decreased in the treatment groups. Caspase-3 activity and DNA fragmentation increased while monocyte adhesion and ICAM-1/VCAM-1 levels decreased significantly. Among subcomponents of EGb761, kaemferol and quercetin reduced VSMC migration and increased caspase activity. Conclusions EGb761 has a protective role in the development of atherosclerosis and is a potential therapeutic agent for preventing atherosclerosis.
Obesity Indices Related to Obstructive Sleep Apnea in Obese Adults  [PDF]
Jongwoo Kim, Seon Yeong Lee
Journal of Biosciences and Medicines (JBM) , 2017, DOI: 10.4236/jbm.2017.510004
Abstract: Background: Obstructive Sleep Apnea (OSA) is prevalent in obese patients. OSA should be evaluated because it might increase mortality. We aimed to evaluate the risk for OSA in obese Korean adults, and to examine the obesity indices most strongly associated with OSA. Method: Anthropometric measurements, fat computed tomography (CT) and dual energy X-ray absorptiometry (DEXA) were performed in 30 obese patients. All patients were divided into low or high risk group of OSA using Berlin Questionnaire. We compared differences between the groups in obesity-related indices. Result: Eleven of the 30 patients (36.7%) were in the low OSA risk group and 19 (63.3%) were in the high OSA risk group. The correlation coefficients for BMI, neck circumference, and neck-to-height ratio × 100(%) in the high-risk group versus the low-risk group were 1.03, 1.96, and 4.04, respectively (P = 0.03). Conclusion: The obesity index most strongly associated with OSA was neck circumference to height ratio.
Cardiovascular Risk Factors and Epicardial Adipose Tissue Measured by Chest Computed Tomography in Healthy Adults  [PDF]
Jongwoo Kim, Seon Yeong Lee
Journal of Biosciences and Medicines (JBM) , 2017, DOI: 10.4236/jbm.2017.511006
Abstract: Background: Epicardial adipose tissue (EAT) may produce several cytokines contributed to coronary atherosclerosis. EAT was measured by transthoracic echocardiography or 3 dimensional cardiac computed tomography (CT) on previous studies. We aimed to evaluate the correlation between EAT thickness and cardiovascular risk factors in healthy adults. Method: We collected clinical, biochemical information from 469 subjects (371 men and 98 women) who visited our health promotion center. EAT thickness was measured by chest CT on the free wall of the right ventricle. Result: The mean EAT thickness was 2.47 ± 1.64 mm in total of 469 subjects. EAT thickness was significantly correlated to age, weight, body mass index (BMI), total body fat, systolic and diastolic blood pressure, total cholesterol, low density lipoprotein (LDL)-cholesterol, and fasting glucose in men and to age, height, weight, BMI, total body fat, systolic and diastolic blood pressure, triglycerides, C-reactive protein (CRP), and fasting glucose in women. Multivariate analysis showed that age, BMI, systolic blood pressure, fasting glucose were the variables that independently correlated to EAT thickness in men. But there was no significant independent variable in women. Conclusion: In our study, EAT thickness measured with chest CT in healthy individuals correlates with cardiovascular risk factors in men.
Effect of a Dipeptidyl Peptidase-IV Inhibitor, Des-Fluoro-Sitagliptin, on Neointimal Formation after Balloon Injury in Rats
Soo Lim, Sung Hee Choi, Hayley Shin, Bong Jun Cho, Ho Seon Park, Byung Yong Ahn, Seon Mee Kang, Ji Won Yoon, Hak Chul Jang, Young-Bum Kim, Kyong Soo Park
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035007
Abstract: Background Recently, it has been suggested that enhancement of incretin effect improves cardiac function. We investigated the effect of a DPP-IV inhibitor, des-fluoro-sitagliptin, in reducing occurrence of restenosis in carotid artery in response to balloon injury and the related mechanisms. Methods and Findings Otsuka Long-Evans Tokushima Fatty rats were grouped into four: control (normal saline) and sitagliptin 100, 250 and 500 mg/kg per day (n = 10 per group). Sitagliptin or normal saline were given orally from 1 week before to 2 weeks after carotid injury. After 3 weeks of treatment, sitagliptin treatment caused a significant and dose-dependent reduction in intima-media ratio (IMR) in obese diabetic rats. This effect was accompanied by improved glucose homeostasis, decreased circulating levels of high-sensitivity C-reactive protein (hsCRP) and increased adiponectin level. Moreover, decreased IMR was correlated significantly with reduced hsCRP, tumor necrosis factor-α and monocyte chemoattractant protein-1 levels and plasminogen activator inhibitor-1 activity. In vitro evidence with vascular smooth muscle cells (VSMCs) demonstrated that proliferation and migration were decreased significantly after sitagliptin treatment. In addition, sitagliptin increased caspase-3 activity and decreased monocyte adhesion and NFκB activation in VSMCs. Conclusions Sitagliptin has protective properties against restenosis after carotid injury and therapeutic implications for treating macrovascular complications of diabetes.
Soluble Expression of Human Leukemia Inhibitory Factor with Protein Disulfide Isomerase in Escherichia coli and Its Simple Purification
A. Song Jung, Bon-Kyung Koo, Seon-Ha Chong, Kyunhoo Kim, Dong Kyu Choi, Thu Trang Thi Vu, Minh Tan Nguyen, Boram Jeong, Han-Bong Ryu, Injune Kim, Yeon Jin Jang, Robert Charles Robinson, Han Choe
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0083781
Abstract: Human leukemia inhibitory factor (hLIF) is a multifunctional cytokine that is essential for maintaining the pluripotency of embryonic stem cells. hLIF may be also be useful in aiding fertility through its effects on increasing the implantation rate of fertilized eggs. Thus these applications in biomedical research and clinical medicine create a high demand for bioactive hLIF. However, production of active hLIF is problematic since eukaryotic cells demonstrate limited expression and prokaryotic cells produce insoluble protein. Here, we have adopted a hybrid protein disulfide isomerase design to increase the solubility of hLIF in Escherichia coli. Low temperature expression of hLIF fused to the b'a' domain of protein disulfide isomerase (PDIb'a') increased the soluble expression in comparison to controls. A simple purification protocol for bioactive hLIF was established that includes removal of the PDIb'a' domain by cleavage by TEV protease. The resulting hLIF, which contains one extra glycine residue at the N-terminus, was highly pure and demonstrated endotoxin levels below 0.05 EU/μg. The presence of an intramolecular disulfide bond was identified using mass spectroscopy. This purified hLIF effectively maintained the pluripotency of a murine embryonic stem cell line. Thus we have developed an effective method to produce a pure bioactive version of hLIF in E. coli for use in biomedical research.
Development of an HbA1c-Based Conversion Equation for Estimating Glycated Albumin in a Korean Population with a Wide Range of Glucose Intolerance
Chang Hee Jung, You-Cheol Hwang, Kwang Joon Kim, Bong Soo Cha, Cheol-Young Park, Won Seon Jeon, Jae Hyeon Kim, Sang-Man Jin, Sang Youl Rhee, Jeong-taek Woo, Byung-Wan Lee
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0095729
Abstract: Background Compared to the golden standard glycation index of HbA1c, glycated albumin (GA) has potentials for assessing insulin secretory dysfunction and glycemic fluctuation as well as predicting diabetic vascular complications. However, the reference ranges of GA and a conversion equation need to be clearly defined. We designed this study to determine the reference ranges in patients with normal glucose tolerance (NGT) based on conventional measures of glycemic status and to devise a conversion equation for calculating HbA1c and GA in a Korean population. Methodology/Principal Findings In this multicenter, retrospective, cross-sectional study, we recruited antidiabetic drug-na?ve patients with available glycemic variables including HbA1c, GA, and fasting plasma glucose regardless of glucose status. For the reference interval of serum GA, 5th to 95th percentile value of GA in subjects with NGT was adopted. The conversion equation between HbA1c and GA was devised using an estimating regression model with unknown break-points method. The reference range for GA was 9.0–14.0% in 2043 subjects. The 95th percentile responding values for FPG, and HbA1c were approximately 5.49 mmol/l, and 5.6%, respectively. The significant glycemic turning points were 5.868% HbA1c and 12.2% GA. The proposed conversion equation for below and above the turning point were GA (%) = 6.960+0.8963 × HbA1c (%) and GA (%) = ?9.609+3.720 × HbA1c (%), respectively. Conclusions/Significance These results should be helpful in future studies on the clinical implications of high GA relative to HbA1c and the clinical implementation of diabetes management.
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