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

Qiang Shi, Gene B. Hubbard, Rampratap S. Kushwaha, David Rainwater, Charles A. Thomas, M. Michelle Leland, John L. VandeBerg, Xing L. Wang

Research output: Contribution to journalArticlepeer-review

23 Scopus citations


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 β-galactosidase activities (SA-β-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-β-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.

Original languageEnglish (US)
Pages (from-to)H2913-H2920
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number6
StatePublished - Jun 2007
Externally publishedYes


  • Intercellular adhesion molecule
  • Senescence-associated β-galactosidase
  • Vascular cell adhesion molecule

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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