Biological trace element research
-
Biol Trace Elem Res · Nov 2016
Zn2+ and mPTP Mediate Endoplasmic Reticulum Stress Inhibition-Induced Cardioprotection Against Myocardial Ischemia/Reperfusion Injury.
The purpose of this study was to determine whether Zn2+ is involved in endoplasmic reticulum (ER) stress inhibition-induced cardioprotection against ischemia/reperfusion (I/R) injury by modulation of the mitochondrial permeability transition pore (mPTP) opening. Isolated rat hearts were subjected to 30-min regional ischemia followed by 2 h of reperfusion. Expression of glucose regulated protein 78 (GRP 78 or BIP), an ER homeostasis marker, was not increased during ischemia but was increased upon reperfusion, indicating that ER stress was initiated upon reperfusion but not during ischemia. ⋯ In support, TUDCA significantly increased intracellular free zinc. These data suggest that reperfusion but not ischemia initiates ER stress and inhibition of ER stress protects the heart from reperfusion injury through prevention of the mPTP opening. Increased intracellular free Zn accounts for the cardioprotective effect of ER stress inhibition.