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• W3024134509 abstract "Macrophage foam cells (i.e., cholesteryl ester-laden macrophages) are abundant in atherosclerotic plaques, and increased macrophage foam cell content is associated with plaque instability (1, 2). Macrophages are generally thought to unload surplus cholesterol via efflux mediated by the ATP-binding cassette transporters A1 and G1 (ABCA1 and ABCG1) to apolipoprotein A1 [apoA1 (3, 4)] and high-density lipoproteins [HDLs (5, 6)], respectively. Several studies in large-population cohorts have shown that the cholesterol efflux capacity of HDL (i.e., its potential to act as an acceptor for cholesterol efflux from macrophages) is an inverse predictor of cardiovascular disease (7⇓–9), highlighting the importance of cholesterol efflux as an atheroprotective mechanism.In PNAS, He et al. (10) describe a mechanism for macrophage cholesterol efflux, which involves the transfer of surplus cholesterol from the macrophage plasma membrane to the plasma membrane and cytosolic lipid droplets of adjacent smooth muscle cells (SMCs). This transcellular cholesterol movement (TCM) could represent a mode that macrophages and perhaps other cell types use to unload excessive cholesterol, helping to prevent potential toxicity associated with excessive cholesterol accumulation and in atherosclerotic plaques helping to reverse the formation of macrophage foam cells. The discovery of TCM was made possible by the use of sophisticated technology (nano-secondary ion mass spectrometry [NanoSIMS] imaging) that allows microscopic colocalization of 13C-cholesterol with 15N-choline (11). As such, the transfer of 13C-cholesterol from macrophages to adjacent SMCs that were metabolically labeled with 15N-choline could be imaged (15N-choline is incorporated into the SMC membrane components phosphatidylcholine and sphingolipids). Within atherosclerotic plaques, macrophages or monocytes could unload their surplus cholesterol onto adjacent SMCs, leading to reversal of macrophage foam cell formation, which … [↵][1]1To whom correspondence may be addressed. Email: m.westerterp{at}umcg.nl or art1{at}cumc.columbia.edu. [1]: #xref-corresp-1-1" @default.
• W3024134509 created "2020-05-21" @default.
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• W3024134509 date "2020-05-18" @default.
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• W3024134509 title "A new pathway of macrophage cholesterol efflux" @default.
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• W3024134509 doi "https://doi.org/10.1073/pnas.2007836117" @default.
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