Impaired PI3K/Akt signaling as a potential cause of failure to precondition rat hearts under conditions of simulated hyperglycemia

Title:

Impaired PI3K/Akt signaling as a potential cause of failure to precondition rat hearts under conditions of simulated hyperglycemia

Creator:

Zálešák, M., Blažíček, P., Gablovský, I., Ledvényiová, V., Monika Barteková, Atila Ziegelhöffer, and Ravingerová, T.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:a00f2502-0610-4287-b22f-5cddf20025a4
uuid:a00f2502-0610-4287-b22f-5cddf20025a4
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, proteinové kinázy, protein kinases, phosphatidylinositol 3-kinase (PI3K), Protein kinase B (Akt), Ischemic preconditioning, simulated hyperglycemia, bcl-2-like protein 4 (BAX), 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

The aim of the study was to evaluate the impact of simulated acute hyperglycemia (HG) on PI3K/Akt signaling in preconditioned and non -preconditioned isolated rat hearts perfused with Krebs -Henseleit solution containing normal (11 mmol/l) or elevated (22 mmol/l) glucose subjected to ischemia -reperfusion. Ischemic preconditioning (IP) was induced by two 5 -min cycle s of coronary occlusion followed by 5 -min reperfusion. Protein levels of Akt, phosphorylated (activated) Akt (P-Akt), as well as contents of BAX protein were assayed (Western blotting) in cytosolic fraction of myocardial tissue samples taken prior to and a fter 30 -min global ischemia and 40- min reperfusion. In “normoglycemic ” conditions (NG), IP significantly increased P -Akt at the end of long -term ischemia, while reperfusion led to its decrease together with the decline of BAX levels as compared to non- pre conditioned hearts. On the contrary, under HG conditions, P -Akt tended to decline in IP - hearts after long -term ischemia, and it was significantly higher after reperfusion than in non -preconditioned controls . No significant influence of IP on BAX levels at the end of I/R was observed under HG conditions . It seems that high glucose may influence IP -induced activation of Akt and its downstream targets, as well as maintain persistent Akt activity that may be detrimental for the heart under above conditions., M. Zálešák, P. Blažíček, I. Gablovský, V. Ledvényiová, M. Barteková, A. Ziegelhöffer, T. Ravingerová., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2015 Volume:64 | Number:5

Harvested from:

CDK

Metadata only:

false