Preconditioning by 17beta-estradiol in isolated rat heart depends on PI3-K/PKB pathway, PKC, and ROS

American Journal of Physiology. Heart and Circulatory Physiology
Mikhail A SovershaevKirsti Ytrehus

Abstract

To study the cell signaling events leading to 17beta-estradiol (E(2))-induced acute cardioprotection, we subjected isolated rat hearts to three 5-min cycles of 10 microM E(2) before 30 min of regional ischemia, followed by 2 h of reperfusion. Protection was judged by changes in infarct size in percentage of risk zone volume. To test the importance of phosphoinositide 3-kinase (PI3-K), protein kinase C (PKC), or reactive oxygen species (ROS) in E(2)-induced protection, we combined wortmannin (1 microM), chelerythrine (2 microM), and 2-mercaptopropionylglycine (300 microM), respectively, with E(2) exposure. Changes in phosphorylation of protein kinase B (PKB) and selected PKC isoforms were tested by immunoblotting of total lysates and subcellular fractions, along with assessment of PKC translocation from soluble to membrane fraction of heart tissue homogenates. Intracellular ROS levels induced by E(2) preconditioning were investigated. E(2) preconditioning led to significant reduction in infarct size from 31.8 +/- 5.3 to 20.2 +/- 2.6% in male hearts and from 42.7 +/- 4.7 to 17.1 +/- 3.4% in female hearts (P < 0.05). Protection was abolished by wortmannin (30.0 +/- 3.2%), chelerythrine (45.1 +/- 4.4%), and 2-mercaptopropionylglyci...Continue Reading

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Citations

Feb 19, 2013·Pflügers Archiv : European journal of physiology·Paula-Anahi Arias-LozaTheo Pelzer
Jul 5, 2011·Clinical and Experimental Pharmacology & Physiology·James R BellLea Md Delbridge
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Jun 1, 2017·Journal of Orthopaedic Research : Official Publication of the Orthopaedic Research Society·Levente PócsAndrea Szabó
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Dec 22, 2019·British Journal of Pharmacology·Marisol Ruiz-MeanaKirsti Ytrehus

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