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Hyperosmotic Stimulus Down-regulates 1α, 25-dihydroxyvitamin D3- induced Osteoclastogenesis by Suppressing the RANKL Expression in a Co-culture System
YuShunTian, HyunJooJeong, Sang-DoLee, SeokHeuiKong, Seung-HoOhk, Yun-JungYoo, Jeong-TaegSeo, DongMinShin, Byung-WhaSohn, Syng-IllLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2010, Vol.14 No.3 9 169-176 (8 pages)
as a mechanical factor for bone remodeling. However, whether the hyperosmotic stimulus affects 1Ձ, 25-dihydroxyvitamin D3 (1Ձ,25(OH)2D3)-induced osteoclastogenesis is not clear. In the present study, the effect of the hyperosmotic stimulus on 1Ձ,25(OH)2D3- induced osteoclastogenesis was investigated in an osteoblast-preosteoclast co-culture system. Serial doses of sucrose were applied as a mechanical force. These hyperosmotic stimuli significantly evoked a reduced number of... -
Redox Factor-1 Inhibits Cyclooxygenase-2 Expression via Inhibiting of p38 MAPK in the A549 Cells
DaeGoonYoo, CukSeongKim, SangKiLee, HyoShinKim, EunJungCho, MyoungSooPark, SangDoLee, JinBongPark, ByeongHwaJeon 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2010, Vol.14 No.3 4 139-144 (6 pages)
In this study, we evaluated the role of apurinic/apyrimidinic endonuclease1/redox factor-1 (Ref-1) on the tumor necrosis factor-Ձ (TNF-Ձ) induced cyclooxygenase-2 (COX-2) expression using A549 lung adenocarcinoma cells. TNF-Ձ induced the expression of COX-2 in A549 cells, but did not induce BEAS-2B expression. The expression of COX-2 in A549 cells was TNF-Ձ dose-dependent (5∼100 ng/ml). TNF-Ձ-stimulated A549 cells evidenced increased Ref-1 expression in a... -
The Inhibitory Effects of Hydrogen Sulfide on Pacemaker Activity of Interstitial Cells of Cajal from Mouse Small Intestine
ShankarPrasadParajuli, SeokChoi, JunLee, YoungDaeKim, ChanGukPark, ManYooKim, HyunIlKim, CheolHoYeum, JaeYeoulJun 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2010, Vol.14 No.2 4 83-89 (7 pages)
In this study, we studied whether hydrogen sulfide (H2S) has an effect on the pacemaker activity of interstitial cells of Cajal (ICC), in the small intestine of mice. The actions of H2S on pacemaker activity were investigated using whole-cell patch-clamp technique, intracellular Ca2+ analysis at 30oC and RT-PCR in cultured mouse intestinal ICC. Exogenously applied sodium hydrogen sulfide (NaHS), a donor of hydrogen sulfide, caused a slight tonic inward current on pacemaker activity in ICC at... -
Inhibition of eNOS/sGC/PKG Pathway Decreases Akt Phosphorylation Induced by Kainic Acid in Mouse Hippocampus
SangHyunLee, JongSeonByun, PilJaeKong, HeeJaeLee, DukKyungKim, HaeSungKim, Jong-HeeSohn, JaeJunLee, , SoYoungLim, WanjooChun, SungSooKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2010, Vol.14 No.1 6 37-43 (7 pages)
The serine/threonine kinase Akt has been shown to play a role of multiple cellular signaling pathways and act as a transducer of many functions initiated by growth factor receptors that activate phosphatidylinositol 3-kinase (PI3K). It has been reported that phosphorylated Akt activates eNOS resulting in the production of NO and that NO stimulates soluble guanylate cyclase (sGC), which results in accumulation of cGMP and subsequent activation of the protein kinase G (PKG). It has been also... -
Overexpression of Ref-1 Inhibits Lead-induced Endothelial Cell Death via the Upregulation of Catalase
KwonHoLee, SangKiLee, HyoShinKim, EunJungCho, HeeKyoungJoo, EunJiLee, JiYoungLee, MyoungSooPark, SeokJongChang, Chung-HyunCho, JinBongPark 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2009, Vol.13 No.6 4 431-436 (6 pages)
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... -
Arachidonic Acid Activates K+-Cl?-cotransport in HepG2 Human Hepatoblastoma Cells
YongSooLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2009, Vol.13 No.5 11 401-408 (8 pages)
K+-Cl−-cotransport (KCC) has been reported to have various cellular functions, including proliferation and apoptosis of human cancer cells. However, the signal transduction pathways that control the activity of KCC are currently not well understood. In this study we investigated the possible role of phospholipase A2 (PLA2)-arachidonic acid (AA) signal in the regulatory mechanism of KCC activity. Exogenous application of AA significantly induced K+ efflux in a dose-dependent manner, which... -
Inhibition of β-amyloid1-40 Peptide Aggregation and Neurotoxicity by Citrate
YongHoonPark, Young-JinKim, IlHongSon, HyunDukYang 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2009, Vol.13 No.4 2 273-279 (7 pages)
The accumulation of Ղ-amyloid (AՂ) aggregates is a characteristic of Alzheimer's disease (AD). Furthermore, these aggregates have neurotoxic effects on cells, and thus, molecules that inhibit AՂ aggregate formation could be valuable therapeutics for AD. It is well known that aggregation of AՂ depends on its hydrophobicity, and thus, in order to increase the hydrophilicity of AՂ, we considered using citrate, an anionic surfactant with three carboxylic acid groups. We... -
Kainic Acid-induced Neuronal Death is Attenuated by Aminoguanidine but Aggravated by L-NAME in Mouse Hippocampus
Jong-SeonByun, Sang-HyunLee, Seong-HoJeon, Yong-SooKwon, HeeJaeLee, Sung-SooKim, Young-MyeongKim, Myong-JoKim, WanjooChun 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2009, Vol.13 No.4 1 265-271 (7 pages)
death with concomitant decreases in iNOS expression and microglial activation. The protective effect of aminoguanidine was maintained for up to 2 weeks. Furthermore, iNOS knockout mice (iNOS−/−) were resistant to KA-induced neuronal death. The present study demonstrates that aminoguanidine attenuates KA-induced neuronal death, whereas L-NAME aggravates neuronal death, in the CA3 region of the hippocampus, suggesting that NOS isoforms play different roles in KA-induced excitotoxicity. -
Block of hERG K+ Channel by Classic Histamine H1 Receptor Antagonist Chlorpheniramine
Hee-KyungHong, Su-HyunJo 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2009, Vol.13 No.3 12 215-220 (6 pages)
Chlorpheniramine is a potent first-generation histamine H1 receptor antagonist that can increase action potential duration and induce QT prolongation in several animal models. Since block of cardiac human ether-a-go-go-related gene (hERG) channels is one of leading causes of acquired long QT syndrome, we investigated the acute effects of chlorpheniramine on hERG channels to determine the electrophysiological basis for its proarrhythmic potential. We examined the effects of chlorpheniramine on... -
Zinc Inhibits Amyloid β Production from Alzheimer's Amyloid Precursor Protein in SH-SY5Y Cells
JinuLee, ChulHoonKim, DongGooKim, YoungSooAhn 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2009, Vol.13 No.3 9 195-200 (6 pages)
Zinc released from excited glutamatergic neurons accelerates amyloidՂ(AՂ)aggregation, underscoring the therapeutic potential of zinc chelation for the treatment of Alzheimer's disease (AD). Zinc can also alter AՂconcentration by affecting its degradation. In order to elucidate the possible role of zinc influx in secretase-processed AՂproduction, SH-SY5Y cells stably expressing amyloid precursor protein (APP) were treated with pyrrolidine dithiocarbamate (PDTC), a zinc...


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