Visit our Expo - Redox and Inflammation signaling 2012

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Session II : Receptor signaling and G proteins Poster II, 41 Endoglin modulates Transforming Growth Factor-beta signaling pathways in L6E9 myoblasts Alicia Rodríguez-Barbero, Soraya Velasco, José M. López-Novoa Instituto Reina Sofía de Investigación Nefrológica. Dpto de Fisiología y Farmacología. Universidad de Salamanca. Campus Unamuno, Edificio Departamental. Avda. Campo Charro s/n. 37007. Salamanca. Spain. E-mail: barberoa@usal.es Endoglin is a transmembrane accessory receptor for transforming growth factor-# (TGF-#). TGF-# elicits cellular responses via specific type I and II serine/threonine kinase receptors and their downstream nuclear effectors, termed Smads. Type I receptors act downstream of type II receptors and determine the signalling specificity within the receptor complex. In most cells, TGF-# signals via TGF-# type II receptor and activin receptor-like kinase (ALK) 5 to induce Smad2/3 phosphorylation. However, it has recently been shown that in endothelial cells TGF-# activates two distinct types I receptor pathways, that is, ALK5-inducing Smad2/3 phosphorylation and ALK1-promoting Smad1/5 phosphorylation. Endoglin, as well as other TGF-# signaling components, is involved in several pathophysiological processes such as angiogenesis and fibrosis. Mutations in endoglin and ALK1 have been linked to the vascular disorder, hereditary hemorrhagic telangiectasia type 1 (HHT1). However, the function of endoglin in TGF-#/ALK signalling has remained unclear. To assess the function of endoglin in TGF-#/ALK signalling, we select a non-endoglin expressed cell type such as L6E9 rat myoblasts, and transfected them with L-endoglin. We found that both, the classic TGF- #/ALK5 and the endothelial specific TGF-#/ALK1 pathways are present and functional in L6E9 myoblasts. TGF-#1 activated both Smad1 y Smad2/3 and also induced Smad2/3 and Smad4 nuclear translocation without differences between mock and endoglin transfected myoblasts. Nevertheless, endoglin promote Id1 expression and reduce PAI-1 activity. Our results indicate a pivotal role for endoglin in the balance of ALK1 and ALK5 signalling. The progression in our understanding on the functional role of endoglin might have important relevance in the regulation of pathophysiological processes in which endoglin is involved. - 168 -
Session II : Receptor signaling and G proteins Poster II, 42 Galphaz subunits are essential partners for permanent association of receptor-activated Galphai subunits to RGS9-2 proteins. María Rodríguez-Muñoz, David Bermúdez, Elena de la Torre-Madrid, Pilar Sánchez- Blázquez and Javier Garzón. Laboratorio de Neurofarmacología. Instituto Cajal. Avenida Doctor Arce 37, 28002 Madrid. Spain. Email: mrodriguez@cajal.csic.es The in vivo administration of an ED80 of morphine induces the transfer of mu-opioid receptors (MOR) that are associated with Galpha subunits to RGS9-2 proteins (1). The phosphorylation of specific residues in or near the RGS box and the subsequent binding to 14- 3-3 impedes RGS9-2 GAP activity and stabilizes this interaction. Thus, by retaining MORactivated Galphai2 subunits, RGS9-2 proteins play a key role in the onset of opioid tolerance. Besides the role of RGS9-2 in these processes, morphine also promotes the association of Galpha subunits with RGS-Z proteins. Since recent studies have shown that Galphaz subunits are stably associated with RGSZ2, we have examined the contribution of Galphaz to the sequestering of Galphai subunits by RGS9-2 proteins. Proteins from mouse PAG synaptosomal membranes were immunoprecipitated with anti-RGS9-2 IgGs and analysed by Western blotting. An anti Phospho-Serine antiserum recognised a 76Kda protein that corresponded to RGS9-2. Impairing the expression of Galphaz through the subchronic administration of selective ODNs provoked a 45% reduction in the Ser phosphorylation of RGS9-2 and reduced tolerance to repeated administration of morphine. Conversely, in Galphai2 knockdown animals and mice receiving exogenous Galphaz subunits, the phosphorylation of RGS9-2 augmented by 36 and 42%, respectively. Our data show that activated GalphazGTP subunits are required for agonist-dependent phosphorylation of RGS9- 2 proteins, which leads to the stabilization and sequestering of MOR-activated G-alpha subunits by RGS9-2 proteins. (Supported by MEC SAF2003-01121 and BMC2002-03228;Instituto de Salud Carlos III G03/005) 1. Garzón J, Rodríguez-Muñoz M, López-Fando A, Sánchez-Blázquez P (2005) J. Biol. Chem. 280: 8951-8960 - 169 -
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- 1 - Luxembourg, January 25th to 2
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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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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 XI : Cell death and cardiov
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Session XI: Cell death and cardiova
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Session XIII : Cell signaling pathw
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Session XV : Reactive oxygen specie
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Session XVI : Chemopreventive agent
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Session XVII : Cell signaling in he
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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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Dr. Jochen Hefl Division of Signal
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Mr. Jan Jepsen 2100 Copenhagen DNK
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