Brief report: Increased apoptosis in advanced atherosclerotic lesions of Apoe-/- mice lacking macrophage Bcl-2

Edward Thorp, Yankun Li, Liping Bao, Pin Mei Yao, George Kuriakose, James Rong, Edward A. Fisher, Ira Tabas*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

67 Scopus citations

Abstract

Objective-Macrophage apoptosis plays important roles in atherosclerosis. Bcl-2 is a key cell survival molecule, but its role in macrophage apoptosis in atherosclerosis is not known. The goal herein was to determine the effect of macrophage-targeted deletion of Bcl-2 on macrophage apoptosis in atherosclerotic lesions of Apoe-/- mice. Methods and Results-Bcl2flox-LysMCre mice were created as a model of macrophage Bcl-2 deficiency. Macrophages from these mice were more susceptible to apoptosis than those from control Bcl WT-LysMCre mice. The mice were bred onto the Apoe-/- background and fed a Western-type diet for 4 or 10 weeks. Apoptotic cells were equally very rare in the lesions of both groups of the 4-week-diet mice, and there was no difference in lesion area. However, Bcl2flox- LysMCre;Apoe-/- plaques from the 10-week-diet protocol had a 40% to 45% increase in apoptotic cells and, in female mice, a ≈25% increase in plaque necrosis (P<0.05) compared with Bcl2WTLysMCre lesions. Conclusions-Macrophage Bcl-2 plays a protective role against macrophage apoptosis specifically in advanced atherosclerotic lesions of Apoe-/- mice.

Original languageEnglish (US)
Pages (from-to)169-172
Number of pages4
JournalArteriosclerosis, thrombosis, and vascular biology
Volume29
Issue number2
DOIs
StatePublished - Feb 2009

Keywords

  • Animal models of human disease
  • Apoptosis
  • Atherosclerosis-pathophysiology
  • Macrophage

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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