Activation of members of the mitogen-activated protein (MAP) kinase family and their downstream effectors has been proposed to play a key role in the pathogenesis of cell survival, ischaemic preconditioning, @entity1283 and @entity712 . This study investigated the responses of @entity70181 kinase and multiple MAP kinases during the transition from compensated pressure-overload @entity1184 to decompensated @entity712 . Extracellular signal-regulated protein kinase (ERK) 1/2, p38, and @entity70181 were activated by chronic pressure-overload and their activity was sustained for 8 weeks after aortic banding. In contrast, while p90 ribosomal S6 kinase (90RSK) and big MAP kinase 1 (BMK1) were activated in compensated @entity1184 , their activities were significantly decreased in hearts with @entity712 . No changes were found in C-Jun @entity2733 terminal kinase (JNK) activity after aortic banding. These data suggest that differential activation of MAP kinase family members may contribute to the transition from compensated to decompensated @entity1184 . We also examined acute effects of mechanical stretch on the activation of these kinases in normal and @entity1184 hearts. In the isolated coronary-perfused heart, a balloon in the left ventricle was inflated to achieve minimum end-diastolic pressure of 25 mmHg for 10-20 min. In normal @entity840 hearts, stretch activated ERK1/2, p90RSK, p38, @entity70181 , and BMK1 but not JNK. However in @entity1184 hearts, further activation of these kinases was not observed by acute mechanical stretch. Mechanical stretch-induced activation of ERK1/2 and p38 kinase in normal hearts was attenuated significantly by a protein kinase C inhibitor, @entity668 . We demonstrate that ERK1/2, p90RSK, p38, @entity70181 , and BMK1 are activated by chronic pressure-overload and by acute mechanical stretch. These data suggest that @entity70181 , BMK1 and p90RSK play a role as novel signal transduction pathways leading to @entity1283 . In addition, the differential inhibition of p90RSK and BMK1 in hearts with @entity712 suggests the specific role of these two kinases to maintain cardiac function under chronic pressure-overload.

@entity70181 and multiple MAP kinase activation in XXXX and @entity712 under chronic pressure-overload: comparison with acute mechanical stretch.

@entity70181 :: ('100728509', 'Gene') :: ['Src'] @entity712 :: ('MESH:D006333', 'Disease') :: ['congestive heart failure', 'heart failure'] @entity1184 :: ('MESH:D006984', 'Disease') :: ['hypertrophy', 'hypertrophied'] @entity1283 :: ('MESH:D006332', 'Disease') :: ['cardiac hypertrophy'] @entity840 :: ('10141', 'Species') :: ['guinea pig'] @entity668 :: ('MESH:C016299', 'Chemical') :: ['chelerythrine'] @entity2733 :: ('CHEBI:29345', 'Chemical') :: ['NH2']
@entity1283 :: (MESH:D006332,Disease) :: ['cardiac hypertrophy']
