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Editorial
. 2014 Jun;34(6):e11-2.
doi: 10.1161/ATVBAHA.114.303553. Epub 2014 Apr 17.

Anti-inflammatory effects of high-density lipoprotein through activating transcription factor 3: benefit beyond cholesterol transport-dependent processes

Hanrui Zhang  1 , Muredach P Reilly  2
Affiliations
Editorial

Anti-inflammatory effects of high-density lipoprotein through activating transcription factor 3: benefit beyond cholesterol transport-dependent processes

Hanrui Zhang et al. Arterioscler Thromb Vasc Biol. 2014 Jun.
No abstract available

Keywords: HDL cholesterol; commentary; inflammation.

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Figures

Figure 1
Figure 1. Vascular directed anti-inflammatory effects of HDL
HDL inhibits expression of adhesion molecules in endothelial cells (EC), ameliorates monocyte activation and adhesion to endothelial monolayer, reduces expression of monocyte chemoattractant protein-1 (MCP-1) in vascular smooth muscle cells (VSMC), suppresses bone marrow hematopoietic stem and multipotential progenitor cells (HSPC) proliferation and leukocytosis. In macrophages, toll like receptor (TLRs) ligands stimulate transcription of inflammatory molecules. HDL suppresses TLR ligand-induced inflammation via activation of Atf3, which serves as a negative regulator of TLR signaling. ATF3 accumulates on the promoters of TLR-stimulated inflammatory genes and represses gene transcription. In contrast to effects on TLR1/2 and TLR9 signaling, HDL can also directly neutralize the inflammatory activity of the TLR4 ligand, lipopolysaccharide (LPS). In cholesterol-loaded macrophages (not shown), HDL can suppress inflammation by promoting cholesterol efflux, thereby reducing free cholesterol (FC) accumulation in plasma membrane lipid rafts and ameliorating cholesterol crystal-induced inflammasome activation.
See this image and copyright information in PMC

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