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p66shc Adaptor Protein Suppresses the Activation of Endothelial Nitric Oxide Synthase in Mouse Embryonic Fibroblasts
SangKiLee, YoungShinKim, CukSeongKim, SookJinSon, DaeGoonYoo, KwonHoLee, SangDoLee, JinBongPark, ByeongHwaJeon 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.3 7 155-160 (6 pages)
Among the Shc proteins, p66shc is known to be related to oxidative stress responses and regulation of the production of reactive oxygen species (ROS). The present study was undertaken to investigate the role of p66shc on endothelial nitric oxide synthase (eNOS) activity in the mouse embryonic fibroblasts (MEFs). When wild type (WT) or p66shc (/) MEFs were transfected with full length of eNOS cDNA, the expression and activity of eNOS protein were higher in the p66shc... -
Protective Effect of Defibrotide on Splanchnic Injury following Ischemia and Reperfusion in Rats
SooRanChoi, JiHoonJeong, JinHoSong, YongKyooShin 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 10 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.2 5 85-94 (10 pages)
A splanchic artery occlusion for 90 min followed by reperfusion of the mesenteric circulation resulted in a severe form of circulatory shock, characterized by endothelial dysfunction, severe hypotension, marked intestinal tissue injury, and a high mortality rate. The effect of defibrotide, a complex of single-stranded polydeoxyribonucleotides having antithrombotic effect, was investigated in a model of splanchnic artery occlusion (SAO) shock in urethane anesthetized rats. Occlusion of the... -
Conditioned Medium from Dying Smooth Muscle Cell Induced Apoptotic Death
MoonHyunBu, KyeongAhLee, KoanHoiKim, ByungYongRhim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2005, Vol.9 No.6 1 315-322 (8 pages)
In this study, the authors investigated whether death of vascular smooth muscle cell (VSMC) had a pathological pertinence. Conditioned media obtained from rat aorta smooth muscle cell (SMC) that were induced death by expressing FADD in the absence of tetracycline (FADD-SMC) triggered death of normal SMC. DNA fragmentation and caspase-3 activation were observed in dying SMC by conditioned media. FADD-SMC showed transcriptional activation of tumor necrosis factor (TNF)-α. Conditioned medium... -
YS 49, a Synthetic Isoquinoline Alkaloid, Protects Sheep Pulmonary Artery Endothelial Cells from tert-butylhydroperoxide-mediated Cytotoxicity
WonSeogChong, SunYoungKang, YoungJinKang, MinKyuPark, YoungSooLee, HyeJungKim, HanGeukSeo, JaeHeunLee, HyeSookYun-Choi, KiChurlChang 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2005, Vol.9 No.5 5 283-290 (8 pages)
Endothelium, particularly pulmonary endothelium, is predisposed to injury by reactive oxygen species (ROS) and their derivatives. Heme oxygenase (HO) has been demonstrated to provide cytoprotective effects in models of oxidant-induced cellular and tissue injuries. In the present study, we investigated the effects of YS 49 against oxidant [tert-butylhydroperoxide (TBH)]-induced injury using cultured sheep pulmonary artery endothelial cells (SPAECs). The viability of SPAECs was determined by... -
Androgen Hormone Inhibits Expression of iNOS and COX-2 Protein in Rat Vascular Smooth Muscle Cell
HwaYoungBae, JiEunPark, EunMiJeon, YoungJinKang, KwangYounLee, HyoungChulChoi 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2005, Vol.9 No.4 5 215-222 (8 pages)
testosterone and dihydrotestosterone suppressed LPS induced iNOS and COX-2 protein expression. RT-PCR analysis revealed that testosterone and dihydrotestosterone did not inhibit mRNA expression of iNOS and COX-2 stimulated by 24 hours of LPS incubation. Proliferation rate was slower in VSMC treated with testosterone and dihydrotestosterone. Testosterone enhanced androgen receptor expression, and LPS significantly reduced androgen receptor protein expression in VSMC. These results indicate that... -
What is the Key Step in Muscle Fatty Acid Oxidation after Change of Plasma Free Fatty Acids Level in Rats?
Kyung-OhDoh, Sang-DugSuh, Jong-YeonKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2005, Vol.9 No.3 7 173-178 (6 pages)
The purpose of this study was to discern the critical point in skeletal muscle fatty acid oxidation by changing plasma free fatty acids (FFA) level in rat. In the study, 3 key steps in lipid oxidation were examined after changing plasma FFA level by acipimox. The rates of both palmitate and palmitoyl- carnitine oxidation were decreased by decrease of plasma FFA level, however, carnitine palmitoyl transferase (CPT) 1 activity was not changed, suggesting CPT1 activity may not be involved in the... -
Inhibition of Angiotensin II-Induced Vascular Smooth Muscle Cell Hypertrophy by Different Catechins
YingZheng, HyeJinSong, SeokHeeYun, YeonJeongChae, HaoJia, ChanHyungKim, TaeSunHa, AgapiosSachinidis, HeeYulAhn, SraT.Davidge 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2005, Vol.9 No.2 7 117-124 (8 pages)
used to assess VSMC hypertrophy, protein kinase assay, and western blot analysis were used to assess mitogen-activated protein kinase (MAPK) activity, and RT-PCR was used to assess c-jun or c-fos transcription. Ang II increased [3H]-leucine incorporation into VSMC. However, EGCG and ECG, but not EGC or EC, inhibited [3H]-leucine incorporation increased by Ang II. Ang II increased phosphorylation of c-Jun, extracellular-signal regulated kinase (ERK) 1/2 and p38 MAPK in VSMC, however, EGCG and ECG... -
Mechanisms of Myotonic Dystrophies 1 and 2
TimchenkoLubov 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2005, Vol.9 No.1 1 1-8 (8 pages)
Myotonic Dystrophies type 1 and 2 (DM1/2) are neuromuscular disorders which belong to a group of genetic diseases caused by unstable CTG triplet repeat (DM1) and CCTG tetranucleotide repeat (DM2) expansions. In DM1, CTG repeats are located within the 3' untranslated region of myotonin protein kinase (DMPK) gene on chromosome 19q. DM2 is caused by expansion of CCTG repeats located in the first intron of a gene coding for zinc finger factor 9 on chromosome 3q. The CTG and CCTG expansions are... -
Effect of Defibrotide on Rat Reflux Esophagitis
HyoungKiKim, SooRanChoi, SangJinChoi, MyungSupChio, YongKyooShin 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 10 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2004, Vol.8 No.6 5 319-328 (10 pages)
This study was aimed at evaluating the effect of defibrotide on the development of the surgically induced reflux esophagitis, on gastric secretion, lipid peroxidation, polymorphonuclear leukocytes (PMNs) accumulation, polymorphonuclear leukocytes adherence, superoxide anion and hydrogen peroxide production in PMNs, scavenge of hydroxyl radical and hydrogen peroxide, cytokine (interleukin-1β, tumor necrosis factor-α) production in blood, and intracellular calcium mobilization in PMNs.... -
Inhibition of Inducible Nitric Oxide Synthase Expression by YS 49, a Synthetic Isoquinoline Alkaloid, in ROS 17/2.8 Cells Activated with TNF-α, IFN-γ and LPS
YoungJinKang, SunYoungKang, YoungSooLee, MinKyuPark, HyeJungKim, HanGeukSeo, JaeHeunLee, HyeSookYun-Choi, KiChurlChang 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2004, Vol.8 No.5 6 273-280 (8 pages)
by Northern and Western blot analysis, respectively. The underlying mechanism by which YS 49 suppressed iNOS expression was not to affect iNOS mRNA stability but to inhibit activation and translocation of NF-κB by preventing the degradation of its inhibitory protein IκBα. As expected, YS 49 prevented NO-induced apoptotic cell death by sodium nitroprusside. Taken together, it is concluded that YS 49 inhibits iNOS expression by interfering with degradation of phosphorylated inhibitory κBα...


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