Format

Send to:

Choose Destination
See comment in PubMed Commons below
Curr Opin Lipidol. 2012 Oct;23(5):471-8. doi: 10.1097/MOL.0b013e328356f967.

Apolipoprotein E regulation of myeloid cell plasticity in atherosclerosis.

Author information

  • 1Department of Surgery, University of California San Francisco, and Veterans Affairs Medical Center, San Francisco, California 94121, USA. robert.raffai@ucsfmedctr.org

Abstract

PURPOSE OF REVIEW:

Apolipoprotein (apo) E is a multifunctional protein that has long been recognized for its ability to safeguard against atherosclerosis. Among its pleiotropic roles known to suppress atherosclerosis, mechanisms by which apoE regulates cells of the immune system have remained elusive. Because atherosclerosis is a chronic inflammatory disease that remains on the rise, understanding in more detail how apoE controls immune cell activation and function is of much interest.

RECENT FINDINGS:

Literature reported in the past year introduces apoE as a regulator of monocyte and macrophage plasticity. Through signals delivered by its interaction with cell surface receptors, apoE has been shown to influence the polarity and inflammatory phenotypes of the macrophage. By promoting cellular cholesterol efflux in a cell autonomous manner and through its ability to enhance HDL function in hyperlipidemic plasma, apoE is now known to suppress atherosclerosis by controlling myeloid cell proliferation, monocyte activation and their capacity to infiltrate the vascular wall. Lastly, the structural basis for apoE isoform-specific effects in macrophage dysfunction and atherosclerosis susceptibility is beginning to emerge.

SUMMARY:

Collectively, these findings introduce a new dimension to our understanding of how apoE links lipoprotein biology to monocyte and macrophage function in atherosclerosis susceptibility.

PMID:
22892903
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Lippincott Williams & Wilkins
    Loading ...
    Write to the Help Desk