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Título : | Role of the alpha2-isoform of AMP-activated protein kinase in the metabolic response of the heart to no-flow ischemia |
Creador: | Zarrinpashneh E |
Nivel de acceso: | Open access |
Palabras clave : | Proteínas Quinasas Activadas por AMP - metabolismo - ratones Acetil-CoA Carboxilasa - metabolismo - ratones Adenina - análisis - ratones Adenosina Trifosfato - metabolismo - ratones Ácidos Grasos - metabolismo - ratones Regulación Enzimológica de la Expresión Génica - fisiología - ratones Glucógeno - metabolismo - ratones Isoenzimas - fisiología - ratones Lactatos - metabolismo - ratones Ratones Noqueados - Ratones Complejos Multienzimáticos - metabolismo - ratones Contracción Miocárdica - fisiología - ratones Isquemia Miocárdica - enzimología - ratones Miocardio - enzimología - ratones Fenotipo - genética - ratones Proteínas Quinasas -genetics - ratones Proteínas Quinasas - metabolismo - ratones Proteínas Serina-Treonina Quinasas - metabolismo - ratones AMP-Activated Protein Kinases Acetyl-CoA Carboxylase -metabolism - Mice Adenine - analysis - Mice Adenosine Triphosphate -metabolism - Mice Fatty Acids - metabolism - Mice Gene Expression Regulation, Enzymologic physiology - Mice Glycogen -metabolism - Mice Isoenzymes - physiology - Mice Lactates - metabolism - Mice Mice, Knockout - Mice Multienzyme Complexes metabolism -Mice Myocardial Contraction physiology - Mice Myocardial Ischemia -enzymology - Mice Myocardium - enzymology- Mice Phenotype Protein Kinases - genetics - Mice Protein Kinases - metabolism - Mice Protein-Serine-Threonine Kinases - metabolism - Mice |
Descripción : | AMP-activated protein kinase (AMPK) is a major sensor and regulator of the energetic state of the cell. Little is known about the specific role of AMPKalpha(2), the major AMPK isoform in the heart, in response to global ischemia. We used AMPKalpha(2)-knockout (AMPKalpha(2)(-/-)) mice to evaluate the consequences of AMPKalpha(2) deletion during normoxia and ischemia, with glucose as the sole substrate. Hemodynamic measurements from echocardiography of hearts from AMPKalpha(2)(-/-) mice during normoxia showed no significant modification compared with wild-type animals. In contrast, the response of hearts from AMPKalpha(2)(-/-) mice to no-flow ischemia was characterized by a more rapid onset of ischemia-induced contracture. This ischemic contracture was associated with a decrease in ATP content, lactate production, glycogen content, and AMPKbeta(2) content. Hearts from AMPKalpha(2)(-/-) mice were also characterized by a decreased phosphorylation state of acetyl-CoA carboxylase during normoxia and ischemia. Despite an apparent worse metabolic adaptation during ischemia, the absence of AMPKalpha(2) does not exacerbate impairment of the recovery of postischemic contractile function. In conclusion, AMPKalpha(2) is required for the metabolic response of the heart to no-flow ischemia. The remaining AMPKalpha(1) cannot compensate for the absence of AMPKalpha(2) |
Colaborador(es) u otros Autores: | Carjaval K Ginion A Beauloye C Mateo P Pouleur Ap Horman S Vaulont S Hoerter J Viollet B Hue L Vanoverschelde Lj Bertrand L. |
Fecha de publicación : | 2006 |
Tipo de publicación: | Artículo |
Formato: | |
Identificador del Recurso : | 10.1152/ajpheart.01032.2005 |
Fuente: | Am J Physiol Heart Circ Physiol 291(6):H2875-H2883 |
URI : | http://repositorio.pediatria.gob.mx:8180/handle/20.500.12103/2777 |
Idioma: | eng |
Aparece en las colecciones: | Artículos |
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