This Article Free upon publication Full Text Full Text (PDF) All Versions of this Article: 29/2/153    most recent ATVBAHA.108.179903v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Clarke, M. C.H. Articles by Bennett, M. R. Search for Related Content PubMed PubMed Citation Articles by Clarke, M. C.H. Articles by Bennett, M. R. Related Collections Related Article

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2009;29:153.)
© 2009 American Heart Association, Inc.

Editorials

Cause or Consequence

What Does Macrophage Apoptosis Do in Atherosclerosis?

Murray C.H. Clarke; Martin R. Bennett

From the Division of Cardiovascular Medicine, University of Cambridge, Addenbrooke’s Centre for Clinical Investigation, Addenbrooke’s Hospital, UK.

Correspondence to Professor Bennett, Division of Cardiovascular Medicine, University of Cambridge, Box 110, Addenbrooke’s Centre for Clinical Investigation, Addenbrooke’s Hospital, Cambridge CB2 2QQ, UK. E-mail mrb@mole.bio.cam.ac.uk

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Cell death is found in human and animal atherosclerotic plaques.^1–4 There is now extensive evidence for both apoptosis and necrosis, the latter being either a primary process or secondary to apoptosis (secondary necrosis). There is also extensive evidence that other processes or structural changes in the plaque accompany cell death, such as inflammation, thrombosis, calcification, and changes in size of both the fibrous cap and necrotic core (reviewed in⁵). Plaque cell death is also associated with a systemic proinflammatory state, with changes in multiple serum cytokines.^6–8 However, the most difficult problem has been determining just what the cause and effect relationship is between cell death and these processes. Fortunately, studies performed over recent years have begun to directly address this problem.

See accompanying article on page 169

Apoptosis is detectable in atherosclerosis, with increasing frequencies as the plaque develops.⁴ Thus, the consequences of apoptosis are likely to be more important in advanced rather than early plaques. However, even this simple assumption may not be correct. The first problem relates to detection and measurement of apoptosis in plaques. Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) or cleaved caspase-3 antibodies are most frequently used to detect apoptotic cells. However, it is not clear how much of the apoptotic process is detectable using these systems: clearly, if cleaved caspase-3 antigen is only detectable for part of the time the cell is undergoing apoptosis, measurement of the cleaved enzyme alone will underestimate the frequency. Similarly, the presence of TUNEL-positive bodies long after apoptosis . . . [Full Text of this Article]

Related Article:

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, and Ira Tabas
Arterioscler Thromb Vasc Biol 2009 29: 169-172. [Abstract] [Full Text] [PDF]