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The Akt1 isoform is an essential mediator of ischaemic preconditioning.

Kunuthur SP, Mocanu MM, Hemmings BA, Hausenloy DJ, Yellon DM - J. Cell. Mol. Med. (2012)

Bottom Line: Phosphatidyl-inositol-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.Akt1 but not Akt2 is essential for mediating a protective response to an IPC stimulus.

View Article: PubMed Central - PubMed

Affiliation: The Hatter Cardiovascular Institute, The Institute of Cardiovascular Science, University College London, London, UK.

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Quantitative analysis of myocardial infarct areas expressed as a percentage of areas at risk in (A) Akt1 and (B) Akt2 transgenic mice. Backward slashes denote values from mice subjected to ischaemia-reperfusion (I-R) injury without an ischaemic preconditioning (IPC) stimulus and forward slashes denote those subjected to either 1 cycle of IPC (IPC1) or three cycles of IPC (IPC3). Values are expressed as means ± S.E.M.; N = 6–10; *P ≤ 0.05 compared to I-R of the same genotype.
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fig03: Quantitative analysis of myocardial infarct areas expressed as a percentage of areas at risk in (A) Akt1 and (B) Akt2 transgenic mice. Backward slashes denote values from mice subjected to ischaemia-reperfusion (I-R) injury without an ischaemic preconditioning (IPC) stimulus and forward slashes denote those subjected to either 1 cycle of IPC (IPC1) or three cycles of IPC (IPC3). Values are expressed as means ± S.E.M.; N = 6–10; *P ≤ 0.05 compared to I-R of the same genotype.

Mentions: Ischaemia-reperfusion injury did not result in larger myocardial infarct areas in mice lacking either one or both alleles for the Akt1 gene compared to their littermate control mice (Fig. 3A). We then proceeded to examine whether Akt1 plays a role in mediating the ischaemic preconditioning stimulus. Ischaemic preconditioning resulted in significant protection in Akt1+/+ mice against I-R injury (28.9 ± 1.4% with IPC versus 45.5 ± 2.6% in control, n = 6, P = 0.0001, Fig. 3A, first panel). However, neither Akt1+/− nor Akt1−/− mice were amenable to protection induced by IPC (40.5 ± 7.8% with IPC versus 45.3 ± 5.1% in control, 38.5 ± 1.9 with IPC versus 42.7 ± 6.5% in control, respectively, n = 6, Fig. 3A, middle panels). In addition, increasing the number of IPC cycles from one to three did not result in significant protection in Akt1+/− mice (32.4 ± 3.2% with IPC versus 41.4 ± 6.3% in control, n = 10, NS, Fig. 3A, last panel).


The Akt1 isoform is an essential mediator of ischaemic preconditioning.

Kunuthur SP, Mocanu MM, Hemmings BA, Hausenloy DJ, Yellon DM - J. Cell. Mol. Med. (2012)

Quantitative analysis of myocardial infarct areas expressed as a percentage of areas at risk in (A) Akt1 and (B) Akt2 transgenic mice. Backward slashes denote values from mice subjected to ischaemia-reperfusion (I-R) injury without an ischaemic preconditioning (IPC) stimulus and forward slashes denote those subjected to either 1 cycle of IPC (IPC1) or three cycles of IPC (IPC3). Values are expressed as means ± S.E.M.; N = 6–10; *P ≤ 0.05 compared to I-R of the same genotype.
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Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3822687&req=5

fig03: Quantitative analysis of myocardial infarct areas expressed as a percentage of areas at risk in (A) Akt1 and (B) Akt2 transgenic mice. Backward slashes denote values from mice subjected to ischaemia-reperfusion (I-R) injury without an ischaemic preconditioning (IPC) stimulus and forward slashes denote those subjected to either 1 cycle of IPC (IPC1) or three cycles of IPC (IPC3). Values are expressed as means ± S.E.M.; N = 6–10; *P ≤ 0.05 compared to I-R of the same genotype.
Mentions: Ischaemia-reperfusion injury did not result in larger myocardial infarct areas in mice lacking either one or both alleles for the Akt1 gene compared to their littermate control mice (Fig. 3A). We then proceeded to examine whether Akt1 plays a role in mediating the ischaemic preconditioning stimulus. Ischaemic preconditioning resulted in significant protection in Akt1+/+ mice against I-R injury (28.9 ± 1.4% with IPC versus 45.5 ± 2.6% in control, n = 6, P = 0.0001, Fig. 3A, first panel). However, neither Akt1+/− nor Akt1−/− mice were amenable to protection induced by IPC (40.5 ± 7.8% with IPC versus 45.3 ± 5.1% in control, 38.5 ± 1.9 with IPC versus 42.7 ± 6.5% in control, respectively, n = 6, Fig. 3A, middle panels). In addition, increasing the number of IPC cycles from one to three did not result in significant protection in Akt1+/− mice (32.4 ± 3.2% with IPC versus 41.4 ± 6.3% in control, n = 10, NS, Fig. 3A, last panel).

Bottom Line: Phosphatidyl-inositol-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.Akt1 but not Akt2 is essential for mediating a protective response to an IPC stimulus.

View Article: PubMed Central - PubMed

Affiliation: The Hatter Cardiovascular Institute, The Institute of Cardiovascular Science, University College London, London, UK.

Show MeSH
Related in: MedlinePlus