Delayed ischemic preconditioning enhances Bcl-2 expression and regulates the mitochondrial permeability transition pore

Second window of ischemic preconditioning regulates mitochondrial permeability transition pore by enhancing Bcl-2 expression.

OBJECTIVE The second window of protection (SWOP) following brief coronary artery occlusion begins at 24 h and may last up to 72 h and occurs via many unknown mechanisms. We investigated the role of the mitochondrial permeability transition pore (PTP), a non specific pore in the inner membrane of the mitochondria in this phenomenon. METHODS Ischemic preconditioning (IP) was induced in Wistar r...

Mitochondrial Transition Pore and Preconditioning 1 Preconditioning Protects by Inhibiting the Mitochondrial Permeability Transition

Antioxidant MCI-186 inhibits mitochondrial permeability transition pore and upregulates Bcl-2 expression.

Reperfusion after a period of ischemia is associated with the formation of reactive oxygen species (ROS) and Ca2+ overload resulting in the opening of a nonspecific pore in the inner membrane of the mitochondria, called the mitochondrial permeability transition pore (PTP), leading to cell damage. Although endogenous antioxidants are activated because of oxidative stress following ischemia, thei...

Transient mitochondrial permeability transition pore opening mediates preconditioning-induced protection.

BACKGROUND Transient (low-conductance) opening of the mitochondrial permeability transition pore (mPTP) may limit mitochondrial calcium load and mediate mitochondrial reactive oxygen species (ROS) signaling. We hypothesize that transient mPTP opening and ROS mediate the protection associated with myocardial preconditioning and mitochondrial uncoupling. METHODS AND RESULTS Isolated perfused ra...

The mitochondrial permeability transition pore regulates endothelial bioenergetics and angiogenesis.

RATIONALE The mitochondrial permeability transition pore is a well-known initiator of cell death that is increasingly recognized as a physiological modulator of cellular metabolism. OBJECTIVE We sought to identify how the genetic deletion of a key regulatory subunit of the mitochondrial permeability transition pore, cyclophilin D (CypD), influenced endothelial metabolism and intracellular sig...