Visit our Expo - Redox and Inflammation signaling 2012

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Session XI: Cell death and cardiovascular diseases Poster XI, 9 Transient and sustained oxidative stress cause differential JNK/SAPK and c-Jun activation in rat cardiac myocytes +nastasia Pechtelidou, Catherine Gaitanaki, and Isidoros Beis Department of Animal and Human Physiology, School of Biology, Faculty of Sciences, University of Athens, Panepistimioupoli, Athens, 157 84, Greece email: ibeis@biol.uoa.gr The aim of the present study was to examine the hypothesis that oxidative stress induces cell death in H9c2 cell line (rat embryonic cardiac myocytes), and to determine whether signalling via JNKs/SAPKs may be involved. We examined the activation of JNKs/SAPKs in response to increasing concentrations of H2O2 (0.04-1 mM), both for the transient and for the sustained oxidative stress. Sustained H2O2 stimulation (0.4 mM) significantly induces maximal phosphorylation of JNKs at 2h, while transient H2O2 stimulation for 5 min induces a maximum phosphorylation of JNKs at 15min after withdrawal. At 2 hours of sustained stimulation peak phosphorylation of the transcription factor c-Jun is also observed, while at the same time significant levels of nuclear activated JNKs are detected. SP600125, the JNK inhibitor II (0.025 mM), abolishes JNK activation induced by 0.4 mM H2O2, as shown by the absence of phosphorylated c-Jun at 2 hours of exposure. For the purpose of measuring cell viability, we used the MTT method. Our results reveal that sustained H2O2 stimulation significantly decreases cell viability, while transient stress does not. Moreover, from the antioxidants tested, only catalase inhibits cell death induced by oxidative stress. Preliminary experiments showed increased Hoechst staining after 24 hours of sustained exposure, but normal nuclear morphology after 5min of stress and 24h withdrawal. In addition, the same pattern of cell morphology is observed under the optical microscope. These results demonstrate an apoptotic type of death under oxidative stress. Based on the above results, we conclude that in H9c2 cells the transient and sustained activation of the JNKs/SAPKs pathway may be differentially involved in cellular signalling during oxidative stress-induced apoptosis. (This study was funded by O.P.E.I.V.T II) - 454 -
Session XI: Cell death and cardiovascular diseases Poster XI, 10 RoY a Novel Synthetic Peptide with Angiogenic and anti Apoptotic properties 1Annat Raiter, 1 Chana Weiss, 1 Orly Kudasi, 2Alexander Battler and 1 Britta Hardy. 1Felsenstein Medical Research Center, Tel-Aviv University School of Medicine, 2Cardiology Dept., Rabin Medical Center, Petah-Tikva, Israel. Email: bhardy@post.tau.ac.il Background: We have identified a novel 12 amino-acid synthetic peptide, RoY, selected from a phage display peptide library by screening against endothelial cells under hypoxia. RoY peptide specifically binds endothelial cells, induces angiogenesis in vitro manifested by proliferation, migration and tube formation. Objectives: to evaluate the therapeutic potential of the synthetic RoY peptide in restoring perfusion in a mouse hind limb ischemic model and to elucidate the mechanism of RoY peptide angiogenic activity under hypoxia by gene expression. Results: Ischemia was created by ligation and excision of the femoral artery in one hind limb of C57BL mice. Seven days after operation, perfusion in the ischemic leg was reduced to 50% in control PBS group, to 65% in RoY peptide group and to 70% in the VEGF group. However, while RoY peptide increased perfusion to 99% at 21 days, perfusion was reduced to 80% with VEGF and remained unchanged with PBS. Gene array, confirmed by RT-PCR, revealed up-regulation of angiogenesis growth factors Angiopoitin-2 and bFGF, Upregulation of chemokine CCL20 and of the anti-apoptotic gene TNF-RSF10D. In contrast, VEGF gene expression in endothelial cells incubated with RoY peptide for 3 or 24 hours was not up-regulated. The percent of apoptosis, measured by FACS analysis, of endothelial cells incubated under hypoxic conditions was inhibited by the addition of RoY peptide from 62% to 33%. Conclusion: RoY is a synthetic peptide that exhibits angiogenic and anti-apoptotic properties under hypoxia by up regulation of growth factors, cytokines and anti apoptotic genes. RoY peptide activity is VEGF independent thus suggests a way to bypass classical VEGF angiogenic system. Treatment of ischemic leg with RoY peptide improved perfusion and walking and climbing function in the mouse. This novel peptide with pro-angiogenic properties may be used as a new therapeutic modality to hypo-vascular diseases. - 455 -
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Table of content PREFACE ..........
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Preface In 1998, we organized the f
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Acknowledgments This meeting has be
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Group B (15h00 - 17h00) Session V.
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- 11 - Exhibition
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Visit our Expo (in alphabetical ord
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Thursday January 26th, 2006 (Early
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Thursday January 26th, 2006 (Evenin
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Regulation of inflammation and gluc
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Saturday January 28th, 2006 (Early
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Oral presentations (by alphabetical
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4: : Lottin S, Vercoutter-Edouart A
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the B-Raf/mitogen-activated/extrace
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Albertini MC, Accorsi A, Citterio B
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AP-1-dependent gene expression in s
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Jaks and cytokine receptors - an in
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The Role of Met-Gab1 Signalling in
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The mammalian tumor suppressor Scri
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SIGNAL TRANSDUCTION BY STRESS-ACTIV
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Title to be announced Caroline Dive
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Mechanisms of DNA methylation in ma
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Blocking the "4 Integrin-Paxillin I
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Regulation of NF-kB-dependent trans
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The immunomodulator AS101 induces g
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Signaling pathways leading to the a
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Boute, N., Jockers, R. and Issad, T
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Jespsen JS, Sorensen MD and Wengel
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8. Nishikawa, H., Kawai, K., Tanaka
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9) Proteome analysis of rat pancrea
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MicroRNA is an anti-apoptotic facto
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Resveratrol inhibits phorbol ester-
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Cross-talk between angiotensin II a
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Multiple role of histamine H 1 rece
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PI3K Targeting by the Beta-GBP Cyto
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D.P. Chopra, R.E. Menard, J. Janusz
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[2] Meijer, L., Flajolet, M. and Gr
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[4] Niemand, C., Nimmesgern, A., Ha
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Oncogenic signaling by mutant p53 M
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activity of the Peroxisome Prolifer
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Restauration of SHIP-1 activity in
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Hypoxia Signaling. Impact on Tumor
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5. Sokolov EI, Zykov KA, Pukhalsky
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HOW ANTITOXIC AND ANTICANCER AGENTS
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Listeria monocytogenes induced Rac1
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Epigenetic Regulation of Stem Cell
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Survey on in vitro cell death induc
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Distinct roles of IRF-3 and IRF-7 i
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Redox-Sensitive Transcription Facto
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Epigenic control of MHC2TA transcri
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Attenuation of MSK1-driven NF-kB ge
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Talking to chromatin: Silencers Sil
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Ubiquitin ligase Smurf1 controls os
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Workshop presentations (by alphabet
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Ambion MicroRNAs (miRNAs) are small
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Organizer: BIOBASE GmbH Date: Janua
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Reliable and efficient gene Knock-d
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Exploring ubiquitin signaling with
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Poster presentations Poster are cla
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Session I : protein domains Poster
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Session II. Receptor signaling and
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Session II : Receptor signaling and
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Session III. Protein kinase cascade
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Session III : Protein kinase cascad
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Session IV. Protein kinase inhibito
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IV. Protein kinase inhibitors: insi
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IV. Protein kinase inhibitors: insi
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V. Phosphatases as key cell signali
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VI. Proteasome degradation pathways
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VI. Proteasome degradation pathways
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Session VII. Stem cell specific cel
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VIII. Inflammation specific signali
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Session IX. Novel compounds targeti
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Session X : Cell death in cancer -
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Session X : Cell death in cancer Po
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Session XV : Reactive oxygen specie
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Session XVI : Chemopreventive agent
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Dr. Nassera Aouali L-1526 Luxembour
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Dr. Giordano Bianchi Clinic of inte
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Mrs. Isabel Burghardt Laboratory of
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Pr. Czeslaw Cierniewski 92-215 Lodz
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Mr. Igotz Delgado Biochemistry 4894
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Dr. Mark Ginsberg Mail code 0726 92
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Dr. Jochen Hefl Division of Signal
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Mr. Jan Jepsen 2100 Copenhagen DNK
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Pr. Young Min Kim Division of Biolo
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Mr. Christoph Lahtz AG Tumorgenetik
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Mrs. Rasa Merzvinskyte Department o
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Dr. Gabriella Regis Tumor Immunolog
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