Role of COX-2 in liver and heart mitochondrial function

Abstract

Liver and heart are two principal organs in the body. Although their physiology is extremely different, both tissues have in common that adult hepatocytes and cardiomyocytes fail to induce COX-2 expression, the key enzyme in the synthesis of prostaglandins, regardless of the pro-inflammatory factors used. In both cell types, COX-2 expression is restricted to those situations in which dedifferentiation or proliferation occur. In parallel studies, using mice genetically modified to selectively express hCOX-2 in hepatocytes [1] and cardiomyocytes [2], we have demonstrated an increased tolerance to ischemia-reperfusion injury (IRI) with an increased functional recovery, a diminished cellular necrosis and less inflammation. It is known that mitochondria have a major role in IRI damage by increasing oxidative stress, decoupling metabolic state and inducing apoptosis. In this work, we analyse different aspects in order to characterize the impact of COX-2 in mitochondrial function.