Cell adhesion
In vitro and animal model studies indicate that the EETs possess anti-inflammatory activity that is directed toward reducing, resolving, and limiting the damage caused by inflammation. Most of these studies have focused on circulating leukocytes, blood vessel endothelium, and the occlusion of blood vessels due to pathological blood clotting. EETs a) inhibit vascular endothelial cells from expressing Cell adhesion molecules such as VCAM-1, ICAM-1, and E-selectin thereby limiting circulating leukocytes from adhering to blood vessel endothelium and migrating across this endothelium into tissues; 2) inhibit the expression and activity of cyclooxygenase-2 in blood monocytes thereby reducing their production of pro-inflammatory metabolites of arachidonic acid such as prostaglandin E2; 3) inhibit platelet aggregation thereby reducing thrombus (i.e. blood clot) formation; 4) promote fibrinolysis thereby dissolving blood clots; and 5) inhibit vascular smooth muscle cell proliferation thereby reducing blood vessel hypertrophy and narrowing.