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      Fish Oil Supplementation Prevents Neointima Formation in Nonhypercholesterolemic Balloon-Injured Rabbit Carotid Artery by Reducing Medial and Adventitial Cell Activation

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          Abstract

          Abstract —We asked whether balloon-injured neointima formation in the presence of high/low serum cholesterol (CT) levels might be affected by dietary supplementation with fish oil (FO). To test this hypothesis, we examined the differentiation, proliferation, or apoptosis profile of smooth muscle cell (SMC) and adventitial cell response to a mild injury induced via a Fogarty catheter in the carotid artery of adult rabbits that had been fed a standard chow or 0.5% CT-enriched diet starting 4 weeks before the lesion. One week before surgery, animals received FO supplementation. This regimen was continued for the following 3 weeks. The effect of FO on the early proliferative/migratory response of carotid SMCs was also examined in 2- and 7-day–injured normocholesterolemic rabbits. As controls, animals subjected to 3-week endothelial injury and animals kept on a 7-week CT diet were used. Carotid cryosections from the various animal groups were evaluated for morphometry (image analysis), differentiation (immunofluorescence with monoclonal antibodies specific for smooth muscle markers, ie, myosin isoforms, SM22, and fibronectin), proliferation (bromodeoxyuridine incorporation), and apoptosis (terminal deoxynucleotidyl transferase–mediated dUTP nick end-labeling). FO treatment significantly reduced the development of intimal thickening in normocholesterolemic rabbits but had no efficacy in the presence of relatively higher serum CT levels. At day 2 (adventitia) and day 7 (neointima, media, and adventitia), the proliferation index of SMCs in FO-treated injured rabbits was markedly lower than in untreated injured controls. Concomitantly with the antiproliferative effect, FO was able to decrease the size of 2 cell types involved in the cell growth response to endothelial injury, namely, the “fetal-type” medial SMC subpopulation and the fibroblast-derived adventitial myofibroblasts. Thus, in our experimental conditions, a low CT level is a permissive condition for FO to prevent neointima formation to a considerable extent. This event is attributable to the early postinjury effect of FO on SMC/adventitial cell proliferation/differentiation patterns.

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          Most cited references27

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          Regulation of differentiation of vascular smooth muscle cells.

          G. Owens (1995)
          The vascular smooth muscle cell (SMC) in mature animals is a highly specialized cell whose principal function is contraction. The fully differentiated or mature SMC proliferates at an extremely low rate and is a cell almost completely geared for contraction. It expresses a unique repertoire of contractile proteins, ion channels, and signaling molecules that are required for its contractile function and that when taken in aggregate clearly distinguish it from any other cell type. During vasculogenesis, however, the SMC's principal function is proliferation and production of matrix components of the blood vessel wall. Moreover, even in mature animals, the SMC retains remarkable plasticity, such that it can undergo relatively rapid and reversible changes in its phenotype in response to changes in local environmental cues normally required for maintenance of its differentiated state. A key to understanding SMC differentiation is to identify the key environmental signals and factors that induce or maintain the differentiated state of the SMC and to determine the molecular mechanisms that control the coordinate expression of genes encoding for proteins that are necessary for the contractile function of the SMC. The purpose of this review is to summarize our current knowledge of the regulation of SMC differentiation, with a particular emphasis on consideration of how this process is controlled during normal vascular development and how these control processes might be altered in vascular diseases such as atherosclerosis, which are characterized by marked alterations in the differentiated state of the SMC.
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            High expression of genes for calcification-regulating proteins in human atherosclerotic plaques.

            Calcification is common in atheromatous plaques and may contribute to plaque rupture and subsequent thrombosis. However, little is known about the mechanisms which regulate the calcification process. Using in situ hybridization and immunohistochemistry we show that two bone-associated proteins, osteopontin (OP) and matrix Gla protein (MGP), are highly expressed in human atheromatous plaques. High levels of OP mRNA and protein were found in association with necrotic lipid cores and areas of calcification. The predominant cell type in these areas was the macrophage-derived foam cell, although some smooth muscle cells could also be identified. MGP was expressed uniformly by smooth muscle cells in the normal media and at high levels in parts of the atheromatous intima. Highest levels of this matrix-associated protein were found in lipid-rich areas of the plaque. The pattern of expression of these two genes contrasted markedly with that of calponin and SM22 alpha, genes expressed predominantly by differentiated smooth muscle cells and whose expression was generally confined to the media of the vessel. The postulated function of OP and MGP as regulators of calcification in bone and the high levels and colocalization of both in atheromatous plaques suggest they have an important role in plaque pathogenesis and stability.
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              The inverse relation between fish consumption and 20-year mortality from coronary heart disease.

              The low death rate from coronary heart disease among the Greenland Eskimos has been ascribed to their high fish consumption. We therefore decided to investigate the relation between fish consumption and coronary heart disease in a group of men in the town of Zutphen, the Netherlands. Information about the fish consumption of 852 middle-aged men without coronary heart disease was collected in 1960 by a careful dietary history obtained from the participants and their wives. During 20 years of follow-up 78 men died from coronary heart disease. An inverse dose-response relation was observed between fish consumption in 1960 and death from coronary heart disease during 20 years of follow-up. This relation persisted after multiple logistic-regression analyses. Mortality from coronary heart disease was more than 50 per cent lower among those who consumed at least 30 g of fish per day than among those who did not eat fish. We conclude that the consumption of as little as one or two fish dishes per week may be of preventive value in relation to coronary heart disease.
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                Author and article information

                Journal
                Arteriosclerosis, Thrombosis, and Vascular Biology
                ATVB
                Ovid Technologies (Wolters Kluwer Health)
                1079-5642
                1524-4636
                January 2000
                January 2000
                : 20
                : 1
                : 152-163
                Affiliations
                [1 ]From the Department of Experimental and Clinical Medicine (E.F., M.P., P.P.) and the Department of Biomedical Sciences (A.C., R.F., S.S.), University of Padua, and the CNR Unit for Muscle Biology and Physiopathology (S.S.), Padua, Italy.
                Article
                10.1161/01.ATV.20.1.152
                ca756e90-8edc-4e34-86d8-5515e75bfe3b
                © 2000
                History

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