Abstract-Elevated plasma levels of the pentraxin protein family member C-reactive protein (CRP) are associated with increased risk of cardiovascular disease in both healthy and high-risk subjects. The long pentraxin family member, pentraxin 3 (PTX3), was recently described. Like CRP, PTX3 is induced by acute inflammatory stimuli and is increased in the blood of patients with acute myocardial infarction. Unlike CRP, it is expressed in a wide range of cell types, but not in hepatocytes. In this study, we have investigated the expression of PTX3 in atherosclerosis. Immunohistochemical staining of advanced atherosclerotic lesions revealed strong expression of PTX3. In contrast, no PTX3 expression was observed in nonatherosclerotic internal mammary arteries. By staining serial sections with cell type-and PTX3-specific antibodies, we observed that PTX3 was produced principally by macrophages and endothelial cells. Key Words: pentraxin 3 Ⅲ atherosclerosis Ⅲ macrophage Ⅲ immunohistochemistry Ⅲ C-reactive protein C ardiovascular disease is the major cause of death in developed countries. 1 Atherosclerosis is the predominant cause of this high incidence of cardiovascular disease. Intimal cholesterol accumulation is a major pathological feature of atherosclerosis, but in recent years there has been a growing understanding of the inflammatory nature of the disease. 2,3 Indeed, the very earliest stages of lesion formation are characterized by an influx of macrophages and T lymphocytes, which become progressively activated during lesion development. 4,5 The precise nature and role of the inflammatory response in atherosclerosis are not fully understood, but they are currently an area of intense research interest because of their potential as diagnostic and therapeutic targets.Studies in animal models have suggested that the inflammatory response associated with atherosclerosis promotes lesion development. 3 This is supported by epidemiological studies in humans. For example, elevations in the plasma concentration of the acute phase protein C-reactive protein (CRP), which is widely used as an indicator of systemic inflammation, correlate with increased risk of cardiovascular disease in both healthy and high-risk subjects. 6 CRP deposition has been detected in atherosclerotic lesions and may enhance lesion development through its ability to activate the complement pathway. 7,8 CRP belongs to the pentraxin protein family, members of which are structurally distinguished by a characteristic pentameric structure. 9 In recent years, a number of new pentraxins have been discovered, including pentraxin 3 (PTX3), neuronal pentraxin 1, and neuronal pentraxin 2. 9 These molecules are known as long pentraxins and are approximately twice the size of the prototypic pentraxins CRP and Serum amyloid P component (SAP). PTX3 was the first long pentraxin to be discovered, and its expression is induced in response to inflammatory stimuli, including tumor necrosis factor (TNF)␣, interleukin (IL)-1␤, and lipopolysaccharide (LPS). 10,11 PTX3 shares ...

In the last 10 years precise cellular functions of alpha-tocopherol, some of which are independent of its antioxidant/radical-scavenging ability, have been revealed. Absorption of alpha-tocopherol from the gut is a selective process. Other tocopherols are not absorbed or are absorbed to a lesser extent. At the post-translational level, alpha-tocopherol inhibits protein kinase C and 5-lipoxygenase and activates protein phosphatase 2A and diacylglycerol kinase. Some genes [platelet glycoprotein IV/thrombospondin receptor/class B scavenger receptor (CD36), alpha-tocopherol transfer protein (alpha-TTP), alpha-tropomyosin, connective tissue growth factor and collagenase] are affected by alpha-tocopherol at the transcriptional level. alpha-Tocopherol also inhibits cell proliferation, platelet aggregation, monocyte adhesion and the oxygen burst in neutrophils. Other antioxidants, such as beta-tocopherol and probucol, do not mimic these effects, suggesting a nonantioxidant, alpha-tocopherol-specific molecular mechanism.

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