The XXXX isoform is an essential mediator of ischaemic preconditioning.

@entity296 @entity6913 @entity6 @entity19 @entity3242 @entity7031 @entity1994 @entity4357 @entity8837
@entity4357 -3-kinase (PI3K)-Akt pathway is essential for conferring cardioprotection in response to ischaemic preconditioning (IPC) stimulus. However, the role of the individual Akt isoforms expressed in the heart in mediating the protective response to IPC is unknown. In this study, we investigated the specific contribution of @entity1994 and @entity3242 in cardioprotection against ischaemia-reperfusion (I-R) injury. @entity19 deficient in @entity1994 or @entity3242 were subjected to in vivo regional @entity296 for 30 min. followed by reperfusion for 2 hrs with or without a prior IPC stimulus. Our results show that @entity19 deficient in @entity1994 were resistant to protection with either one or three cycles of IPC stimulus (42.7    6.5% control versus 38.5    1.9% 1    IPC, N = 6, @entity7031 ; 41.4    6.3% control versus 32.4    3.2% 3    IPC, N = 10, @entity7031 ). Western blot analysis, performed on heart samples taken from @entity1994 (-/-) @entity19 subjected to IPC, revealed an impaired phosphorylation of @entity6913 , a downstream effector of Akt, as well as @entity8837 , the parallel component of the reperfusion injury salvage kinase pathway. @entity3242 (-/-) @entity19 , which exhibit a @entity6 phenotype, however, were amenable to protection with three but not one cycle of IPC (46.4    5.6% control versus 35.9    5.0% in 1    IPC, N = 6, @entity7031 ; 47.0    6.0% control versus 30.8    3.3% in 3    IPC, N = 6; *P = 0.039). @entity1994 but not @entity3242 is essential for mediating a protective response to an IPC stimulus. Impaired activation of @entity6913 and @entity8837 might be responsible for the lack of protective response to IPC in @entity1994 (-/-) @entity19 . The rise in threshold for protection in @entity3242 (-/-) @entity19 might be due to their @entity6 phenotype.
