RISK and SAFE Signaling Pathway Involvement in Apolipoprotein A-I-Induced Cardioprotection
Autor: | Kalakech, Hussein, Hibert, Pierre, Prunier-Mirebeau, Delphine, Tamareille, Sophie, Letournel, Franck, Macchi, Laurent, Pinet, Florence, Furber, Alain, Prunier, Fabrice, Rouet, Philippe |
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Přispěvatelé: | Cardioprotection, Remodelage et Thrombose (CRT), Université d'Angers (UA), UPRES EA 3860, Service Biochimie et Génétique, Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM)-PRES Université Nantes Angers Le Mans (UNAM), Laboratoire de Neurobiologie et Transgénèse (LNBT), Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM), PRES Université Nantes Angers Le Mans (UNAM), Facteurs de Risque et Déterminants Moléculaires des Maladies liées au Vieillissement - U 1167 (RID-AGE), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Laboratoire de Protection et Remodelage du Myocarde (PMRM), Université d'Angers (UA)-Université d'Angers (UA), Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Toulouse (UT)-Université de Toulouse (UT)- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Pinet, Florence, Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM) |
Jazyk: | angličtina |
Rok vydání: | 2014 |
Předmět: |
Pathology
Apolipoprotein B Myocardial Infarction lcsh:Medicine 030204 cardiovascular system & hematology Pharmacology Glycogen Synthase Kinase 3 0302 clinical medicine Cell Signaling GSK-3 Medicine and Health Sciences polycyclic compounds Coronary Heart Disease Phosphorylation lcsh:Science ComputingMilieux_MISCELLANEOUS Cardioprotection 0303 health sciences Multidisciplinary biology [SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system Cardiovascular Diseases Ischemic Preconditioning Myocardial lipids (amino acids peptides and proteins) Signal transduction Research Article Signal Transduction medicine.medical_specialty Cardiotonic Agents Cardiology Myocardial Reperfusion Injury 03 medical and health sciences [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system medicine Animals Rats Wistar GSK3B Protein kinase B 030304 developmental biology Glycogen Synthase Kinase 3 beta Apolipoprotein A-I business.industry Acute Cardiovascular Problems lcsh:R Biology and Life Sciences nutritional and metabolic diseases Cell Biology biology.protein Ischemic preconditioning lcsh:Q business Proto-Oncogene Proteins c-akt |
Zdroj: | PLoS ONE PLoS ONE, Public Library of Science, 2014, 9 (9), pp.e107950. ⟨10.1371/journal.pone.0107950⟩ PLoS ONE, 2014, 9 (9), pp.e107950. ⟨10.1371/journal.pone.0107950⟩ PLoS ONE, Vol 9, Iss 9, p e107950 (2014) |
ISSN: | 1932-6203 |
Popis: | Recent findings indicate that apolipoprotein A-I (ApoA-I) may be a protective humoral mediator involved in remote ischemic preconditioning (RIPC). This study sought to determine if ApoA-I mediates its protective effects via the RISK and SAFE signaling pathways implicated in RIPC. Wistar rats were allocated to one of the following groups. Control: rats were subjected to myocardial ischemia/reperfusion (I/R) without any further intervention; RIPC: four cycles of limb I/R were applied prior to myocardial ischemia; ApoA-I: 10 mg/Kg of ApoA-I were intravenously injected prior to myocardial ischemia; ApoA-I + inhibitor: pharmacological inhibitors of RISK/SAFE pro-survival kinase (Akt, ERK1/2 and STAT-3) were administered prior to ApoA-I injection. Infarct size was significantly reduced in the RIPC group compared to Control. Similarly, ApoA-I injection efficiently protected the heart, recapitulating RIPC-induced cardioprotection. The ApoA-I protective effect was associated with Akt and GSK-3β phosphorylation and substantially inhibited by pretreatment with Akt and ERK1/2 inhibitors. Pretreatment with ApoA-I in a rat model of I/R recapitulates RIPC-induced cardioprotection and shares some similar molecular mechanisms with those of RIPC-involved protection of the heart. |
Databáze: | OpenAIRE |
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