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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: pdf
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
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