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
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