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This Article Full Text Full Text (PDF) All Versions of this Article: 292/6/H2913    most recent 01405.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Shi, Q. Articles by Wang, X. L. Search for Related Content PubMed PubMed Citation Articles by Shi, Q. Articles by Wang, X. L.

Endothelial senescence after high-cholesterol, high-fat diet challenge in baboons

¹Department of Genetics, ³Department of Physiology and Medicine, Southwest Foundation for Biomedical Research; ²Southwest National Primate Research Center, San Antonio; ⁴Cardiothoracic Research Laboratory, Texas Heart Institute, St. Luke's Episcopal Hospital, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston; ⁵Department of Medicine/Division of Hematology, University of Texas Health Science Center, San Antonio, Texas

Submitted 22 December 2006 ; accepted in final form 2 February 2007

Increasing evidence indicates that replicative senescence and premature endothelial senescence could contribute to endothelial dysfunction. This study aims at testing the hypothesis that a high-fat diet may lead to premature vascular endothelial senescence in a nonhuman primate model. We isolated endothelial cells from left and right femoral arteries in 10 baboons before and after a 7-wk high-fat dietary treatment. We compared the morphological alterations, replicative capacities, and senescence-associated -galactosidase activities (SA--gal) at these two time points. We found that high-fat diet increased the prevalence of endothelial senescence. Endothelial replicative capacities declined dramatically, and SA--gal activities increased significantly in postdietary challenge. There was no change in telomeric length using quantitative flow fluorescence in situ hybridization analysis, suggesting that some stressors lead to cell senescence independent of telomere dysfunction. Our findings that high-fat diet causes endothelial damage through the premature senescence suggest a novel mechanism for the diet-induced endothelial dysfunction.

senescence-associated -galactosidase; intercellular adhesion molecule; vascular cell adhesion molecule

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