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"June 21, 2006 | Michael O'Riordan Rome, Italy - One of the possible ways in which long-chain omega-3 fatty acids play a role in decreasing cardiovascular events is by entering advanced atherosclerotic plaques. According to the results of a new study, investigators were able to show that the incorporation of eicosapentaenoic acid (EPA) into advanced plaque was associated with a decreased expression of various matrix metalloproteinases (MMPs) involved in causing plaque instability, as well as with decreased plaque inflammation. These are results of the Omacor Carotid Endarterectomy Intervention (OCEAN) study, presented here this week at the International Symposium on Atherosclerosis by Dr Philip Calder (University of Southampton, UK). "By increasing the availability of omega-3 fatty acids, they appear in advanced atherosclerotic plaques, indicated in this study by the carotid artery, and this results in lower numbers of macrophages, foam cells, and T cells, as well as the lower expression of inflammatory markers," said Calder. "Histologically, this results in a plaque that appears to be less inflamed and more stable. This may contribute to reduced mortality in patients consuming omega-3 fatty acids, for example, in the GISSI Prevenzione trial.""

Induction of ovarian cancer cell apoptosis by 1,25-dihydroxyvitamin D3 through the down-regulation of telomerase. Jiang F, Bao J, Li P, Nicosia SV, Bai W. J Biol Chem. 2004 Dec 17;279(51):53213-21. Epub 2004 Oct 12. PMID: 15485861 doi: 10.1074/jbc.M410395200 Overall, the study suggests that the down-regulation of telomerase activity by 1,25(OH)2VD3 and the resulting cell death are important components of the response of OCa cells to 1,25(OH)2VD3-induced growth suppression. Progressive shortening of telomere associated with cell divisions limits the life span of normal cells and eventually leads to senescence. To become immortal, human cancers including OCa are invariably associated with activation of mechanism that maintains telomere length. Approximately 85-90% of cancers show reactivation of telomerase. The present study shows that telomerase in OCa cells is down-regulated by 1,25(OH)2VD3. Down-regulation of telomerase is due to decreased stability of hTERT mRNA rather than VDRE-mediated transcriptional repression through the putative VDRE present in the regulatory region of the hTERT gene. It is known that the inhibition of telomerase may lead to a phenotypic lag during which cells would continue to divide until the point at which the telomeres became critically short. This phenomenon may explain why the apoptotic induction by 1,25(OH)2VD3 needs the treatment for more than 6 days. As mentioned in the results, no detectable shortening of telomeric repeats was observed in parental OVCAR3 cells after 9 days of treatment with 1,25(OH)2VD3 (Fig. 4D). This is likely due to the fact that the short telomere (about 3 kb) in OVCAR3 cells is very close to the minimal length required for survival and that cells with detectably shorter telomere may have been selected against apoptosis. It has been shown that transformed human cells enter crisis once the terminal restriction fragment of the telomere reaches a length of about 4 kb. This is insufficient to protect chro