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Título : | Dual cardiac contractile effects of the alpha2-AMPK deletion in low-flow ischemia and reperfusion |
Creador: | Carvajal, Karla |
Nivel de acceso: | Open access |
Palabras clave : | Proteínas Quinasas Activadas por AMP - metabolismo Adenosina Trifosfato - metabolismo Respiración de la Célula Forma MM de la Creatina-Quinasa - metabolismo Metabolismo Energético Ácidos Grasos - metabolismo Glucosa - metabolismo Glucógeno - metabolismo Ratones Noqueados Complejos Multienzimáticos - deficiencia Complejos Multienzimáticos - genética Complejos Multienzimáticos - metabolismo Contracción Miocárdica Isquemia Miocárdica - complicaciones Isquemia Miocárdica - genética Isquemia Miocárdica - metabolismo Isquemia Miocárdica - fisiopatologia Daño por Reperfusión Miocárdica - genética Daño por Reperfusión Miocárdica - metabolismo Daño por Reperfusión Miocárdica - fisopatologia Miocardio - enzimología Miocardio - metabolismo Fosfocreatina - metabolismo Fosforilación Proteínas Serina-Treonina Quinasas - deficiencia Proteínas Serina-Treonina Quinasas - genética Proteínas Serina-Treonina Quinasas - metabolismo Ácido Pirúvico - metabolismo AMP-Activated Protein Kinases - metabolism Adenosine Triphosphate - metabolism Cell Respiration Creatine Kinase, MM Form - metabolism Energy Metabolism Fatty Acids -metabolism Glucose - metabolism Glycogen - metabolism Mice, Knockout Multienzyme Complexes - deficiency Multienzyme Complexes - genetics Multienzyme Complexes - metabolism Myocardial Contraction Myocardial Ischemia - complications Myocardial Ischemia - genetics Myocardial Ischemia - metabolism Myocardial Ischemia - physiopathology Myocardial Reperfusion Injury - genetics Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - physiopathology Myocardium - enzymology Myocardium - metabolism Phosphocreatine -metabolism Phosphorylation Protein-Serine-Threonine Kinases - deficiency Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - metabolism Pyruvic Acid - metabolism glucose uptake energetics rigor creatine kinase 31P NMR spectroscopy energetic cost of contractility |
Descripción : | In order to understand if a2-AMPK isoform is a friend or a foe in the protection of the myocardium against ischemia-reperfusion injury, we studied the functional consequence of its deletion on the contractility, the energetics, and the respiration of the isolated perfused heart and characterized the response to low flow ischemia and reperfusion. Alpha2 deletion did not affect basal contractility, respiration and high energy phosphate contents despite a 2 fold reduction in glycogen content and a 3 fold reduction in glucose uptake. Low flow ischemia (LFI) increased AMPK phosphorylation and stimulated glucose uptake and phosphorylation in both a2-KO and WT. The high sensitivity a2-KO to the development of ischemic contracture was attributed to the constitutive impairment in glucose transport and glycogen content and not a perturbation of the energy transfer by creatine kinase (CK). The functional coupling of MM-CK to myofibrillar ATPase and the CK unidirectional fluxes were indeed similar in a2-KO and WT. LFI impaired CK flux by 50% in both strains, suggesting that a2- AMP does not control CK activity. Despite the higher sensitivity to contracture, the post ischemic contractility recovered to 60% of its control in both a2-KO and WT. This could partly result from a low cost of contractility in the a2-KO. In conclusion the a2-AMPK is required for a normal glucose uptake and glycogen content which protects the heart from the development of the ischemic contracture but it is not required for optimal post ischemic recovery of systolic activity in the absence of fatty acids. |
Colaborador(es) u otros Autores: | Elham Zarrinpashneh Ondrej Szarszoi Frederic Joubert Yoni Athea PhilippeMateo Brigitte Gillet Sophie Vaulont Benoit Viollet Xavier Bigard Luc Bertrand Renée Ventura-Clapier Jacqueline A. Hoerter |
Fecha de publicación : | 2007 |
Tipo de publicación: | Artículo |
Formato: | |
Identificador del Recurso : | 10.1152/ajpheart.00683.2006 |
Fuente: | Am J Physiol Heart Circ Physiol 6(192):1--47 |
URI : | http://repositorio.pediatria.gob.mx:8180/handle/20.500.12103/2306 |
Idioma: | eng |
Aparece en las colecciones: | Artículos |
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