Rationale: Immediate changes in the ECM (extracellular matrix) microenvironment occur after myocardial ischemia and reperfusion (I/R) injury.
Objective: Aim of this study was to unravel the role of the early hyaluronan (HA)-rich ECM after I/R.
Methods And Results: Genetic deletion of Has2 and Has1 was used in a murine model of cardiac I/R.
We show that the cyclin-dependent kinase inhibitor 1B (CDKN1B)/p27, previously known as a cell cycle inhibitor, is also localized within mitochondria. The migratory capacity of endothelial cells, which need intact mitochondria, is completely dependent on mitochondrial p27. Mitochondrial p27 improves mitochondrial membrane potential, increases adenosine triphosphate (ATP) content, and is required for the promigratory effect of caffeine.
View Article and Find Full Text PDF