Por favor, use este identificador para citar o enlazar este ítem: http://repositorio.pediatria.gob.mx:8180/handle/20.500.12103/2777
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: PDF
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
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