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Dae Yun Seo,
Sungryul Lee,
Arturo Figueroa,
Hyoung Kyu Kim,
Yeong Ho Baek,
Yi Sub Kwak,
Nari Kim, Tae Hoon Choi,
Byoung Doo Rhee,
Kyung Soo Ko,
Byung Joo Park,
Song Young Park,
Jin Han
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ABSTRACT: Yoga has been known to have stimulatory or inhibitory effects on the metabolic parameters and to be uncomplicated therapy for obesity. The purpose of the present study was to test the effect of an 8-week of yoga-asana training on body composition, lipid profile, and insulin resistance (IR) in obese adolescent boys. Twenty volunteers with body mass index (BMI) greater than the 95th percentile were randomly assigned to yoga (age 14.7±0.5 years, n=10) and control groups (age 14.6±1.0 years, n=10). The yoga group performed exercises three times per week at 40~60% of heart-rate reserve (HRR) for 8 weeks. IR was determined with the homeostasis model assessment of insulin resistance (HOMA-IR). After yoga training, body weight, BMI, fat mass (FM), and body fat % (BF %) were significantly decreased, and fat-free mass and basal metabolic rate were significantly increased than baseline values. FM and BF % were significantly improved in the yoga group compared with the control group (p<0.05). Total cholesterol (TC) was significantly decreased in the yoga group (p<0.01). HDL-cholesterol was decreased in both groups (p<0.05). No significant changes were observed between or within groups for triglycerides, LDL-cholesterol, glucose, insulin, and HOMA-IR. Our findings show that an 8-week of yoga training improves body composition and TC levels in obese adolescent boys, suggesting that yoga training may be effective in controlling some metabolic syndrome factors in obese adolescent boys.
Korean Journal of Physiology and Pharmacology 06/2012; 16(3):175-80. · 0.96 Impact Factor
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Youn Kyoung Son,
Da Hye Hong, Tae-Hoon Choi,
Seong Woo Choi,
Dong Hoon Shin,
Sung Joon Kim,
In Duk Jung,
Yeong-Min Park,
Won-Kyo Jung,
Dae-Joong Kim,
Il-Whan Choi,
Won Sun Park
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ABSTRACT: We investigated the effect of a specific protein kinase C (PKC) inhibitor, bisindolylmaleimide I [BIM (I)], on L-type Ca(2+) channels in rat ventricular myocytes. BIM (I) alone inhibited the L-type Ca(2+) current in a concentration-dependent manner, with a K(d) value of 3.31 ± 0.25 μM, and a Hill coefficient of 2.34 ± 0.23. Inhibition was immediate after applying BIM (I) in the bath solution and then it partially washed out. The steady-state activation curve was not altered by applying 3μ M BIM (I), but the steady-state inactivation curve shifted to a more negative potential with a change in the slope factor. Other PKC inhibitors, PKC-IP and chelerythrine, showed no significant effects either on the L-type Ca(2+) current or on the inhibitory effect of BIM (I) on the L-type Ca(2+) current. The results suggest that the inhibitory effect of BIM (I) on the L-type Ca(2+) current is independent of the PKC pathway. Thus, our results should be considered in studies using BIM (I) to inhibit PKC activity and ion channel modulation.
Biochemical and Biophysical Research Communications 05/2012; 423(1):110-5. · 2.48 Impact Factor
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Hyoung Kyu Kim,
Se Won Kang,
Seung Hun Jeong,
Nari Kim,
Jae Hong Ko,
Hyoweon Bang,
Won Sun Park, Tae-Hoon Choi,
Young-Ran Ha,
Yong Seok Lee,
Jae Boum Youm,
Kyung Soo Ko,
Byoung Doo Rhee,
Jin Han
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ABSTRACT: Ischemic preconditioning (IPC) is a powerful mechanism for limiting myocardial infarction during or after ischemia-reperfusion (IR) injury. However, effective target genes and proteins for IPC are unknown. We characterized global changes in gene expression in the heart during IR, and identified effective target genes for IPC.
Hearts were isolated from Sprague-Dawley rats under control, IR, and IPC conditions. We generated expressed-sequence-tags (ESTs) for each group and investigated their functions and the major biological processes in which they are involved using the eukaryotic clusters of orthologous groups (KOG) database and bioinformatics analysis tools.
IR modified the expression of 126 genes. Of these, 62 were upregulated, 64 were downregulated, and 77 were found to be effective target genes for IPC. In KOG analysis, most of the genes whose expression was modified were involved in energy production and conversion and the cytoskeleton. A gene-to-gene interaction map revealed that IR modified the expression of genes in four major functional modules: electron transport chain/oxidative phosphorylation; tricarboxylic acid cycle/glucose metabolism/amino acid metabolism; cellular structure and contraction; and gene transcription, translation, and protein folding. At the individual gene level, the genes encoding mitochondrial cytochrome c oxidase subunits 2 and 3 were downregulated, and those encoding the major cytoskeleton components tropomyosin, myosin light chain, myomesin 2, and myosin regulatory light chain 2, as well as the gene encoding the iron-storage protein ferritin, were upregulated, and thus were identified as potential target genes. Real time PCR evaluated expression patterns of three mitochondrial IPC effective genes. Two-dimensional electrophoresis proteomic analyses revealed altered expression of 14 target proteins. The expression patterns of six proteins matched the corresponding EST expression patterns.
The global profiling of cardiac ischemia-related genes provides the possible mechanisms of IR and IPC and ways of treating IR injury.
Journal of Cardiology 04/2012; 60(2):98-110. · 1.28 Impact Factor
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Hyoung Kyu Kim,
Won Sun Park,
Mohamad Warda,
So Youn Park,
Eun A Ko,
Min Hee Kim,
Seung Hun Jeong,
Hye-Jin Heo, Tae-Hoon Choi,
Young-Won Hwang,
Sun-Il Lee,
Kyung Soo Ko,
Byoung Doo Rhee,
Nari Kim,
Jin Han
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ABSTRACT: Beta adrenergic overstimulation may increase the vascular damage and stroke. However, the underlying mechanisms of beta adrenergic overstimulation in cerebrovascular dysfunctions are not well known. We investigated the possible cerebrovascular dysfunction response to isoproterenol induced beta-adrenergic overstimulation (ISO) in rabbit cerebral arteries (CAs).
ISO was induced in six weeks aged male New Zealand white rabbit (0.8-1.0 kg) by 7-days isoproterenol injection (300 μg/kg/day). We investigated the alteration of protein expression in ISO treated CAs using 2DE proteomics and western blot analysis. Systemic properties of 2DE proteomics result were analyzed using bioinformatics software. ROS generation and following DNA damage were assessed to evaluate deteriorative effect of ISO on CAs. Intracellular Ca(2+) level change and vascular contractile response to vasoactive drug, angiotensin II (Ang II), were assessed to evaluate functional alteration of ISO treated CAs. Ang II-induced ROS generation was assessed to evaluated involvement of ROS generation in CA contractility.
Proteomic analysis revealed remarkably decreased expression of cytoskeleton organizing proteins (e.g. actin related protein 1A and 2, α-actin, capping protein Z beta, and vimentin) and anti-oxidative stress proteins (e.g. heat shock protein 9A and stress-induced-phosphoprotein 1) in ISO-CAs. As a cause of dysregulation of actin-cytoskeleton organization, we found decreased level of RhoA and ROCK1, which are major regulators of actin-cytoskeleton organization. As functional consequences of proteomic alteration, we found the decreased transient Ca(2+) efflux and constriction response to angiotensin II and high K(+) in ISO-CAs. ISO also increased basal ROS generation and induced oxidative damage in CA; however, it decreased the Ang II-induced ROS generation rate. These results indicate that ISO disrupted actin cytoskeleton proteome network through down-regulation of RhoA/ROCK1 proteins and increased oxidative damage, which consequently led to contractile dysfunction in CA.
PLoS ONE 01/2012; 7(8):e43884. · 4.09 Impact Factor
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ABSTRACT: ATP-sensitive K(+) channels (K(ATP)) are major component of preventing ischemia-reperfusion injury. However, there is little information regarding to the expressional difference of K(ATP) and its function between left and right ventricles. In this study, we measured the lactate dehydrogenase release of rabbit heart slices in vitro and determined the difference of the K(ATP) expression at the both ventricles by measuring the level of K(ATP)-forming Kir6.2 (OcKir6.2) mRNA using in situ hybridization. The hearts were preconditioned with 15 min hypoxia and reoxygenated for 15 min before a hypoxic period of 60 min, followed by reoxygenation for 180 min. With hypoxic preconditioning (100% N(2)) with 15 min, left ventricles (LV) showed higher release of LDH comparing with right ventricles (RV). Adding K(ATP) blocker glibenclamide (10 µM) prior to a hypoxic period of 60 min, hypoxic preconditioning effect of RV was more abolished than LV. With in situ hybridization, the optical density of OcKir6.2 was higher in RV. Therefore, we suggest that different K(ATP) expression between LV and RV is responsible for the different response to hypoxia and hypoxic preconditioning of rabbit hearts.
Korean Journal of Physiology and Pharmacology 08/2011; 15(4):189-94. · 0.96 Impact Factor
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ABSTRACT: We investigated the effects of a hot-water extract of Artemisia iwayomogi, a plant belonging to family Compositae, on cardiac ventricular delayed rectifier K(+) current (I(K)) using the patch clamp technique. The carbohydrate fraction AIP1 dose-dependently increased the heart rate with an apparent EC(50) value of 56.1+/-5.5 microg/ml. Application of AIP1 reduced the action potential duration (APD) in concentration-dependent fashion by activating I(K) without significantly altering the resting membrane potential (IC(50) value of APD(50): 54.80+/-2.24, IC(50) value of APD(90): 57.45+/-3.47 microg/ml). Based on the results, all experiments were performed with 50 microg/ml of AIP1. Pre-treatment with the rapidly activating delayed rectifier K(+) current (I(Kr)) inhibitor, E-4031 prolonged APD. However, additional application of AIP1 did not reduce APD. The inhibition of slowly activating delayed rectifier K(+) current (I(Ks)) by chromanol 293B did not change the effect of AIP1. AIP1 did not significantly affect coronary arterial tone or ion channels, even at the highest concentration of AIP1. In summary, AIP1 reduces APD by activating I(Kr) but not I(Ks). These results suggest that the natural product AIP1 may provide an adjunctive therapy of long QT syndrome.
Korean Journal of Physiology and Pharmacology 06/2010; 14(3):119-25. · 0.96 Impact Factor
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ABSTRACT: We investigated the effect of the phenylalkylamine Ca(2+) channel inhibitor verapamil on voltage-dependent K(+) (Kv) channels in rabbit coronary arterial smooth muscle cells using a whole-cell patch clamp technique. Verapamil reduced the Kv current amplitude in a concentration-dependent manner. The apparent K(d) value for Kv channel inhibition was 0.82 microM. Although verapamil had no effect on the activation kinetics, it accelerated the decay rate of Kv channel inactivation. The rate constants of association and dissociation by verapamil were 2.20+/-0.02 microM(-1) s(-1), and 1.79+/-0.26 s(-1), respectively. The steady-state activation and inactivation curves were unaffected by verapamil. The application of train pulses increased the verapamil-induced Kv channel inhibition. Furthermore, verapamil increased the recovery time constant, suggesting that the inhibitory effect of this agent was use-dependent. The inhibitory effect of verapamil was not affected by intracellular and extracellular Ca(2+)-free conditions. Another Ca(2+) channel inhibitor, nifedipine (10 microM) did not affect the Kv current, and did not alter the inhibitory effect of verapamil. Based on these results, we concluded that verapamil inhibited Kv current in a state-, time-, and use-dependent manner, independent of Ca(2+) channel inhibition.
Biological & Pharmaceutical Bulletin 01/2010; 33(1):47-52. · 1.66 Impact Factor
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ABSTRACT: We investigated the effects of YC-1, an activator of soluble guanylyl cyclase (sGC), on voltage-dependent K+ (Kv) channels in smooth muscle cells from freshly isolated rabbit coronary arteries by using the whole-cell patch clamp technique. YC-1 inhibited the Kv current in a dose-dependent fashion with an apparent K(d) of 9.67 microM. It accelerated the decay rate of Kv channel inactivation without altering the kinetics of current activation. The rate constants of association and dissociation for YC-1 were 0.36 +/- 0.01 microM(-1) x s(-1) and 3.44 +/- 0.22 s(-1), respectively. YC-1 did not have a significant effect on the steady-state activation and inactivation curves. The recovery time constant from inactivation was decreased in the presence of YC-1, and application of train pulses (1 or 2 Hz) caused a progressive increase in the YC-1 blockade, indicating that YC-1-induced inhibition of Kv currents is use-dependent. Pretreatment with Bay 41-2272 (also a sGC activator), ODQ (a sGC inhibitor), or Rp-8-Br-PET-cGMPs (a protein kinase G inhibitor) did not affect the basal Kv current and also did not significantly alter the inhibitory effect of YC-1. From these results, we suggest that YC-1 directly inhibits the Kv current independently of sGC activation and in a state-, time-, and use-dependent fashion.
Journal of Pharmacological Sciences 01/2010; 112(1):64-72. · 2.08 Impact Factor
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ABSTRACT: We examined the effect of the protein tyrosine kinase (PTK) inhibitor, genistein on voltage-dependent K+ (Kv) channels in freshly isolated rabbit coronary arterial smooth muscle cells, using whole-cell patch clamp techniques. The amplitude of the Kv current was inhibited by genistein in a dose-dependent manner, with a Kd value of 7.51 microM. Genistein had no effect on the steady-state activation or inactivation of Kv channels. The applications of trains of pulses at 1 or 2 Hz caused a progressive increase in the genistein-blockade. Genistein produced use-dependent inhibition of the Kv currents, consistent with a slow recovery from inactivation in the presence of genistein. Daidzein and genistin, two inactive analogs of genistein, showed an inhibitory effect similar to that of genistein on Kv channels. Moreover, the absence of ATP inside the pipette did not influence the blocking effect of genistein. We suggest that genistein directly inhibited the Kv current, independently of PTK inhibition.
Vascular Pharmacology 11/2008; 50(1-2):51-6. · 1.99 Impact Factor
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Won Sun Park,
Eun A Ko,
In Duk Jung,
Youn Kyoung Son,
Hyoung Kyu Kim,
Nari Kim,
So Youn Park,
Ki Whan Hong,
Yeong-Min Park, Tae-Hoon Choi,
Jin Han
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ABSTRACT: The effects of angiotensin II (Ang II) on whole-cell large conductance Ca(2+)-activated K(+) (BK(Ca)) currents was investigated in control and Apurinic/apyrimidinic endonuclease1/redox factor 1 (APE1/Ref-1)-overexpressing human umbilical vein endothelial cells (HUVECs). Ang II blocked the BK(Ca) current in a dose-dependent fashion, and this inhibition was greater in APE1/Ref-1-overexpressing HUVECs than in control HUVECs (half-inhibition values of 102.81+/-9.54 nM and 11.34+/-0.39 nM in control and APE1/Ref-1-overexpressing HUVECs, respectively). Pretreatment with the NADPH oxidase inhibitor diphenyleneiodonium (DPI) or knock down of NADPH oxidase (p22 phox) using siRNA increased the inhibitory effect of Ang II on the BK(Ca) currents, similar to the effect of APE1/Ref-1 overexpression. In addition, application of Ang II increased the superoxide and hydrogen peroxide levels in the control HUVECs but not in APE1/Ref-1-overexpressing HUVECs. Furthermore, direct application of hydrogen peroxide increased BK(Ca) channel activity. Finally, the inhibitory effect of Ang II on the BK(Ca) current was blocked by an antagonist of the Ang II type 1 (AT(1)) receptor in both control and APE1/Ref-1-overexpressing HUVECs. From these results, we conclude that the inhibitory effect of Ang II on BK(Ca) channel function is NADPH oxidase-dependent and may be promoted by APE1/Ref-1.
Archives of Pharmacal Research 11/2008; 31(10):1291-301. · 1.59 Impact Factor
