Angiotensin-converting enzyme gene and atherosclerosis

John H. Krege, Jeffrey S. Moyer, Laura L. Langenbach, Li Peng, Sunny H. Zhang, Nobuyo Maeda, Robert L. Reddick, Oliver Smithies

Research output: Contribution to journalArticlepeer-review

18 Scopus citations

Abstract

Common variants of the angiotensin-converting enzyme (ACE) gene (ACE in humans, Ace in mice) associated with changes in circulating ACE activities have been suggested to confer differential risks for atherosclerosis. Using a mouse model of atherosclerosis induced by heterozygosity for apolipoprotein E gene disruption and an atherogenic diet, we have studied the impact on atherogenesis of a mutation that changes the level of function of Ace. We find that this genetically determined change does not influence the size or complexity of atherosclerotic lesions. Ace genotype was not a significant determinant of lesion size in female (+/+=12.9±1.5 and +/-=11.7±1.6 μm 2x10 4) or male (+/+=0.95±0.25 and+/-=1.83±0.59 μm 2x10 4) mice; however, lesions were significantly larger (P<.001) in female than male mice. Ace genotype also did not affect lesion complexity; however, lesions in females showed significantly increased frequency of cholesterol clefts, acellular cores, fibrous caps, and calcifications compared with those in males. The hypothesis that genetic variation in the level of ACE gene expression affects the development of atherosclerosis is not supported by these findings.

Original languageEnglish (US)
Pages (from-to)1245-1250
Number of pages6
JournalArteriosclerosis, Thrombosis, and Vascular Biology
Volume17
Issue number7
StatePublished - 1997
Externally publishedYes

Keywords

  • Apolipoprotein E
  • Arteriosclerosis
  • Dietary cholesterol
  • Gene targeting
  • Renin-angiotensin system

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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