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Identification of Differentially Expressed Genes in Murine Hippocampus by Modulation of Nitric Oxide in Kainic Acid-induced Neurotoxic Animal Model
YoAhnSuh, OMinKwon, SoYoungYim, HeeJaeLee, Sung-SooKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2007, Vol.11 No.4 3 149-154 (6 pages)
Kainic acid (KA) causes neurodegeneration, but no consensus has been reached concerning its mechanism. Nitric oxide may be a regulator of the mechanism. We identified differentially expressed genes in the hippocampus of mice treated with kainic acid, together with or without L-NAME, a nonselective nitric oxide synthase inhibitor, using a new differential display PCR method based on annealing control primers. Eight genes were identified, including clathrin light polypeptide, TATA element... -
A1 Receptor-mediated Protection against Amyloid Beta-induced Injury in Human Neuroglioma Cells
YongWoonCho, HyunJuJung, YongKeunKim, JaeSukWoo 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2007, Vol.11 No.2 1 37-43 (7 pages)
In addition, adenosine prevented Aβ-induced mitochondrial permeability transition, release of cytochrome c into cytosol and subsequent activation of caspase-9. The protective effect of adenosine disappeared when cells were pretreated with 5-hydroxydecanoate, a selective blocker of the mitochondrial ATP-sensitive K channel. In conclusion, therefore we suggest that adenosine exerts protective effect against Aβ-induced cell death of A172 cells, and that the underlying mechanism of the... -
Involvement of Caspases and Bcl-2 Family in Nitric Oxide-Induced Apoptosis of Rat PC12 Cells
Yeon-JinJeong, Ji-YeonJung, Jin-HaLee, Jin-HyoungCho, Guem-SugLee, Sun-HunKim, Won-JaeKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.6 6 329-336 (8 pages)
This study was aimed to investigate the nitric oxide (NO)-induced cytotoxic mechanism in PC12 cells. Sodium nitroprusside (SNP), an NO donor, decreased the viability of PC12 cells in dose- and time- dependent manners. SNP enhanced the production of reactive oxygen species (ROS), and gave rise to apoptotic morphological changes including cell shrinkage, chromatin condensation, and DNA fragmentation. Expression of Bax was not affected, whereas Bcl-2 was downregulated in SNP-treated PC12 cells. SNP... -
Involvement of Bcl-2 Family and Caspases Cascade in Sodium Fluoride-Induced Apoptosis of Human Gingival Fibroblasts
Ji-YeonJung, Jae-HongPark, Yeon-JinJeong, Kyu-HoYang, Nam-KiChoi, Sun-HunKim, Won-JaeKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.5 10 289-294 (6 pages)
Sodium fluoride (NaF) has been shown to be cytotoxic and elicit inflammatory response in human. However, the cellular mechanisms underlying NaF-induced cytotoxicity in periodontal tissues have not yet been elucidated. This study is aimed to investigate the mechanisms of NaF-induced apoptosis in human gingival fibroblast (HGF). NaF decreased the cell viability of HGF in a dose- and time-dependent manner. NaF gave rise to apoptotic morphological changes including cell shrinkage, chromatin... -
Neuroprotective Effects of Lithium on NMDA-induced Excitotoxicity in Mouse Cerebrum
Gee-younKwon, Soo-kyungKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 12 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.3 1 111-122 (12 pages)
Neuroprotective properties of lithium were evaluated by using in vivo NMDA excitotoxicity model. Systemic injection of NMDA to young mice induced neuronal apoptosis mediated by both TNFR-1 and Fas ligand, and long-term lithium treatment showed noticeable neuroprotection against NMDA-induced excitotoxicity: NMDA-damaged neurons expressed several apoptosis-related gene products such as TNFR-1, Fas ligand, and caspase-3, and these gene expressions were not found in the brain of mice chronically... -
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)
the cytotoxicity of MPP against PC12 cells. H2O2 may enhance the MPP-induced viability loss in PC12 cells by promoting the mitochondrial membrane permeability change, release of cytochrome c and subsequent activation of caspase-3, which is associated with the increased formation of ROS and depletion of GSH. The findings suggest that H2O2 as a promoting agent for the formation of mitochondrial permeability transition may enhance the neuronal cell injury caused by neurotoxins. -
Changes of Cytosolic Ca2+ under Metabolic Inhibition in Isolated Rat Ventricular Myocytes
SunghyunKang, NariKim, HyunJoo, JaeBoumYoum, WonSunPark, MohamedWarda, HyungkyuKim, DangVanCuong, TaehoKim, EuiyongKim, JinHan 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2005, Vol.9 No.5 6 291-298 (8 pages)
To characterize cytosolic Ca2 fluctuations under metabolic inhibition, rat ventricular myocytes were exposed to 200μM 2,4-dinitrophenol (DNP), and mitochondrial Ca2, mitochondrial membrane potential (ΔΨm), and cytosolic Ca2 were measured, using Rhod-2 AM, TMRE, and Fluo-4 AM fluorescent dyes, respectively, by Laser Scanning Confocal Microscopy (LSCM). Furthermore, the role of sarcolemmal Na/Ca2 exchange (NCX) in cytosolic Ca2 efflux was studied in... -
Differential Inhibition of MPP+- or 6-Hydroxydopamine-induced Cell Viability Loss in PC12 Cells by Trifluoperazine and W-7
ChungSooLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2005, Vol.9 No.4 9 247-252 (6 pages)
antagonists trifluoperazine and W-7 against the cytotoxicity of MPP and 6-hydroxydopamine (6-OHDA) in relation to the mitochondrial dysfunction and cell death in PC12 cells. Trifluoperazine (an inhibitor of the mitochondrial permeability transition and calmodulin antagonist) and W-7 (a specific calmodulin antagonist) significantly attenuated the MPP- induced cell viability loss in PC12 cells with a maximum inhibition at 0.5∼1μM; beyond these concentrations the inhibitory effect... -
Nitric Oxide-cGMP-Protein Kinase G Pathway Contributes to Cardioprotective Effects of ATP-Sensitive K+ Channels in Rat Hearts
DangVanCuong*, NariKim*, HeeCheolCho, EuiyongKim, JinHan 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2004, Vol.8 No.2 5 95-100 (6 pages)
Ischemic preconditioning (IPC) has been accepted as a heart protection phenomenon against ischemia and reperfusion (I/R) injury. The activation of ATP-sensitive potassium (KATP) channels and the release of myocardial nitric oxide (NO) induced by IPC were demonstrated as the triggers or mediators of IPC. A common action mechanism of NO is a direct or indirect increase in tissue cGMP content. Furthermore, cGMP has also been shown to contribute cardiac protective effect to reduce heart I/R-induced... -
Stretch-activated K+ Channels in Rat Atrial Myocytes
JaeBoumYoum 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2003, Vol.7 No.6 8 341-318 (8 pages)
Mechanical stimuli to the cardiac myocytes initiate many biochemical and physiological events. Stretch-activated cation channels have been suggested to mediate these events. In this study, cell-attached and inside-out excised-patch clamp methods were used to identify stretch-activated cation channels in adult rat atrial myocytes. Channel openings were increased in cell-attached configuration when negative pressure was applied to the pipette, and also in inside-out excised patches by negative...


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