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Mitochondrial calcium uniporter inhibition attenuates mouse bone marrow-derived mast cell degranulation induced by beta-1,3-glucan
DangVanCuong, HyoungKyuKim, JubertMarquez, NariKim, KyungSooKo, ByoungDooRhee, JinHan 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2016, Vol.20 No.2 10 213-220 (8 pages)
, and dynamic changes in cytosolic and mitochondrial calcium and membrane potential were monitored. BG-induced mast cell degranulation occurred in a time-dependent manner, and was significantly reduced under calcium-free conditions. Ruthenium red, a mitochondrial Ca2+ uniporter blocker, significantly reduced mast cell degranulation induced by BG, PGN, and A23187. These results suggest that the mitochondrial Ca2+ uniporter has an important regulatory role in BG-induced mast cell degranulation. -
NecroX-5 protects mitochondrial oxidative phosphorylation capacity and preserves PGC1α expression levels during hypoxia/ reoxygenation injury
VuThiThu, HyoungKyuKim, LeThanhLong, BayalagmaaNyamaa, In-SungSong, ToThanhThuy, NguyenQuangHuy, JubertMarquez, SoonHaKim, NariKim, KyungS 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 11 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2016, Vol.20 No.2 9 201-211 (11 pages)
treatment using an ex vivo Langendorff system. Proteomic analysis was performed using liquid chromatography-mass spectrometry (LC-MS) and non-labeling peptide count protein quantification. Real-time PCR, western blot, citrate synthases and mitochondrial complex activity assays were then performed to assess heart function. Treatment with NecroX-5 during hypoxia significantly preserved electron transport chain proteins involved in oxidative phosphorylation and metabolic functions. NecroX-5 also... -
A Novel Nicotinamide Adenine Dinucleotide Correction Method for Mitochondrial Ca2+ Measurement with FURA-2-FF in Single Permeabilized Ventricular Myocytes of Rat
JeongHoonLee, JeongMiHa, ChaeHunLeem 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 10 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2015, Vol.19 No.4 10 373-382 (10 pages)
carboxy-SNARF-1 for pH were used. With this novel method, we found that the resting mitochondrial [Ca2+] concentration was 1.03 μM. This 1 μM cytosolic Ca2+ could theoretically increase to more than 100 mM in mitochondria. However, the mitochondrial [Ca2+] increase was limited to ∼30 μM in the presence of 1 μM cytosolic Ca2+. Our method solved the problem of NADH signal contamination during the use of Fura-2 analogs, and therefore the method may be useful when NADH interference is expected. -
The Effects of Ischemic Postconditioning on Myocardial Function and Nitric Oxide Metabolites Following Ischemia-Reperfusion in Hyperthyroid Rats
JalalZaman, SajjadJeddi, AsgharGhasemi 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2014, Vol.18 No.6 6 481-488 (8 pages)
Ischemic postconditioning (IPost) could decrease ischemia-reperfusion (IR) injury. It has not yet reported whether IPost is useful when ischemic heart disease is accompanied with co-morbidities like hyperthyroidism. The aim of this study was to examine the effect of IPost on myocardial IR injury in hyperthyroid male rats. Hyperthyroidism was induced with administration of thyroxine in drinking water (12 mg/L) over a period of 21 days. After thoracotomy, the hearts of control and hyperthyroid... -
Cyanidin-3-glucoside Inhibits ATP-induced Intracellular Free Ca2＋ Concentration, ROS Formation and Mitochondrial Depolarization in PC12 Cells
ShaziaPerveen, JiSeonYang, TaeJoungHa, ShinHeeYoon 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 9 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2014, Vol.18 No.4 3 297-305 (9 pages)
inhibited the ATP-induced [Ca2＋]i responses in the presence of nimodipine and ω-conotoxin. Cyanidin-3- glucoside also significantly inhibited KCl (50 mM)-induced [Ca2＋]i increases. Cyanidin-3-glucoside significantly inhibited ATP-induced mitochondrial depolarization. The intracellular Ca2＋ chelator BAPTA-AM or the mitochondrial Ca2＋ uniporter inhibitor RU360 blocked the ATP-induced mito-chondrial depolarization in the presence of cyanidin-3-glucoside. Cyanidin-3-glucoside blocked ATP-... -
A Computational Model of Cytosolic and Mitochondrial [Ca2＋] in Paced Rat Ventricular Myocytes
JaeBoumYoum, SeongWooChoi, ChangHanJang, HyoungKyuKim, ChaeHunLeem, NariKim, JinHan 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 23 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2011, Vol.15 No.4 5 217-239 (23 pages)
of control) of L-type Ca2＋ channel in model simulation, where the relation was reversed. In experiment, block of Ca2＋ uniporter on mitochondrial inner membrane significantly reduced the amplitude of mitochondrial Ca2＋ transients, while it failed to affect the cytosolic Ca2＋ transients. In computer simulation, the amplitude of cytosolic Ca2＋ transients was not affected by removal of Ca2＋ uniporter. The application of carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone (FCCP) known as a... -
Alterations in Membrane Transport Function and Cell Viability Induced by ATP Depletion in Primary Cultured Rabbit Renal Proximal Tubular Cells
SungJuLee, ChaeHwaKwon, YongKeunKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2009, Vol.13 No.1 3 15-22 (8 pages)
in renal proximal tubular cells. ATP depletion was induced by incubating cells with 2.5 mM potassium cyanide (KCN)/0.1 mM iodoacetic acid (IAA), and membrane transport function and cell viability were evaluated by measuring Na＋-dependent phosphate uptake and trypan blue exclusion, respectively. ATP depletion resulted in a decrease in Na＋-dependent phosphate uptake and cell viability in a time-dependent manner. ATP depletion inhibited Na＋-dependent phosphate uptake in cells, when treated with... -
Regional Differences in Mitochondrial Anti-oxidant State during Ischemic Preconditioning in Rat Heart
VuThiThu, DangVanCuong, NariKim, JaeBoumYoum, MohamadWarda, WonSunPark, JaeHongKo, EuiyongKim, JinHan 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2007, Vol.11 No.2 3 57-64 (8 pages)
on mitochondrial function in viable and infarcted cardiac tissues. Our results showed that the mitochondria from viable areas in the IR-induced group were swollen and fused, whereas those in the infarcted area were heavily damaged. IPC protected the mitochondria, thus reducing cardiac injury. We also found that the activity of the mitochondrial antioxidant enzyme system, which includes manganese superoxide dismutase (Mn-SOD), was enhanced in the viable areas compared to the infarcted areas in... -
Monoamine Oxidase Inhibitors Attenuate Cytotoxicity of 1-Methyl-4-phenylpyridinium by Suppressing Mitochondrial Permeability Transition
ChungSooLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.4 7 207-212 (6 pages)
in neuronal cell death. Mitochondrial monoamine oxidase (MAO)-B is considered to play a part in the progress of nigrostriatal cell death. The present study examined the effect of MAO inhibitors against the toxicity of 1-methyl-4- phenylpyridinium (MPP) in relation to the mitochondrial permeability transition. Chlorgyline (a selective inhibitor of MAO-A), deprenyl (a selective inhibitor of MAO-B) and tranylcypromine (non- selective inhibitor of MAO) all prevented cell viability loss,... -
Promoting Effect of Hydrogen Peroxide on 1-Methyl-4-phenylpyridinium-induced Mitochondrial Dysfunction and Cell Death in PC12 Cells
DongHeeLee, ChungSooLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.1 9 51-57 (7 pages)
was assessed by measuring the effect on the mitochondrial membrane permeability. Treatment of PC12 cells with MPP resulted in the nuclear damage, decrease in the mitochondrial transmembrane potential, cytosolic accumulation of cytochrome c, activation of caspase-3, increase in the formation of reactive oxygen species (ROS) and depletion of GSH. Addition of H2O2 enhanced the MPP-induced nuclear damage and cell death. Catalase, Carboxy- PTIO, Mn-TBAP, N-acetylcysteine, cyclosporin A...
