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- W2017384679 abstract "Inactivation of GSK3β via phosphorylation at serine-9 residue has been shown to play a role in ischemic preconditioning. Inhibition of the opening of the mitochondrial permeability transition pore (mPTP) is supposed to be important in pre- and postconditioning. Using GSK-S9A transgenic mice (whose cardiac GSK3β activity cannot be inactivated), we addressed whether postconditioning might require the inactivation of GSK-3β, upstream of the mPTP. Anesthetized wild-type (WT) and GSK-S9A mice underwent 60 min. of LAD occlusion followed by 24 h of reperfusion. WT and GSK-S9A mice were each randomized into 4 groups (n=8–9/g): control (C: no additional intervention), postconditioned (postC: 3 episodes of 1 min. of ischemia followed by 1 min. of reperfusion), CsA (IV bolus injection of 10 mg/kg of ciclosporin A, a mPTP inhibitor) or SB21 (IV bolus injection of SB216763, a GSK3β inhibitor) 1 min before reperfusion. Infarct size was assessed by TTC staining. Area at risk was comparable among groups. In WT mice, infarct size of PostC, SB21 and CsA groups was significantly reduced, averaging 39±3%, 37±4% and 35±5%, respectively, versus 56±5% in C (p<0.05 for all 3 groups). In GSK-S9A mice, infarct size averaged 66±7% in C (p=ns versus WT-C). Infarct size was significantly reduced in CsA, but not postC, groups, averaging 41±8% and 51±5%, respectively. These results suggest that S9-phosphorylation of GSK3β is required for cardioprotection by postconditioning and occurs upstream of the mPTP." @default.
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- W2017384679 date "2007-06-01" @default.
- W2017384679 modified "2023-10-14" @default.
- W2017384679 title "Postconditioning requires inactivation of GSK3β upstream of the mPTP in mice" @default.
- W2017384679 doi "https://doi.org/10.1016/j.yjmcc.2007.03.556" @default.
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