Expression of COX-2 mRNA in Peripheral Blood Monocytes from Patients with Acute Myocardial Infarction and Its Significance

Abstract

Acute myocardial infarction (AMI) may occur when plaque ruptures and leads to thrombosis. Increasing evidence supports the notion that inflammation is involved in the atherogenesis and pathogenesis of AMI (1). Plasma concentrations of several markers of inflammation have been found to be associated with future cardiovascular risk in a variety of clinical settings. These markers include cell adhesion molecules, cytokines, proatherogenic enzymes, and C-reactive protein (CRP). Interleukin-6 (IL-6), a central mediator of the acute-phase response(2), is positively correlated with the risk of future myocardial infarction(3). Matrix metalloproteinase-9 (MMP-9), an important member of the MMP family, may be responsible for the progress of extracellular matrix degradation in atherosclerotic plaques and plays an important role in plaque stability(4)(5). Its substrate types include collagen, which is an essential component of the plaque basement membrane and fibrous cap. Systemic inflammatory markers such as IL-6 and MMP-9 are increased and become important proinflammatory cytokines in patients with AMI(1)(6)(7)(8). Cyclooxygenase-2 (COX-2) is an inducible isoform of COX, which is expressed in very limited fashion throughout most tissues unless induced by inflammatory stimuli or mitogens. COX-2 is the key enzyme that regulates the amount and duration of proinflammatory prostaglandins and plays an important role in inflammation (9)(10). It is now recognized that the antiinflammatory and analgesic actions of nonsteroidal antiinflammatory drugs are largely attributable to inhibition of COX-2 isoenzyme. COX-2 and prostaglandin E2 are known to induce production of the inflammatory cytokine IL-6(11) and promote the release and activation of MMPs(12). Recent studies have shown that expression of COX-2 has also been specifically linked to cardiovascular disease. Because concentrations of the protein are increased in endothelial cells, smooth muscle cells, and macrophages in human atherosclerotic lesions(13)(14 …