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Related Experiment Videos

Elevated plasma membrane cholesterol content alters macrophage signaling and function.

Chunbo Qin1, Tomokazu Nagao, Inna Grosheva

  • 1Department of Biochemistry, Weill Medical College of Cornell University, New York, NY 10021, USA.

Arteriosclerosis, Thrombosis, and Vascular Biology
|November 25, 2005
PubMed
Summary

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Elevated membrane cholesterol in macrophages significantly alters cell behavior, including actin cytoskeleton changes and inhibited migration, offering new insights into early atherogenesis.

Area of Science:

  • Cell Biology
  • Cardiovascular Research
  • Atherosclerosis

Background:

  • Macrophages infiltrate the subendothelial space during atherogenesis.
  • Lipoprotein accumulation transforms macrophages into lipid-laden foam cells.
  • The reason for macrophages retaining lipids in atherosclerotic lesions is unclear.

Purpose of the Study:

  • To test if elevated membrane cholesterol alters macrophage behavior.
  • To investigate the impact of high cholesterol on macrophage functions in the context of atherosclerotic lesions.

Main Methods:

  • J774 macrophages were treated to increase membrane cholesterol using acetylated low-density lipoprotein (ac-LDL) with an ACAT inhibitor or cholesterol-chelated methyl-beta-cyclodextrin (chol-MbetaCD).
  • Effects on cell morphology, actin organization, and adhesion were analyzed.

Related Experiment Videos

  • Macrophage migration was assessed using 3-dimensional transwell chemotaxis assays.

    • Main Results:

    • Increased membrane cholesterol induced dramatic cell ruffling and spreading in J774 macrophages.
    • These morphological changes were dependent on cellular adhesion and involved Rac-mediated signaling.
    • Macrophage migration was significantly inhibited by elevated membrane cholesterol levels.

    Conclusions:

    • Elevated membrane cholesterol profoundly affects macrophage cellular functions, particularly those involving the actin cytoskeleton.
    • These findings provide novel insights into the early cellular mechanisms of atherogenesis.