Apolipoprotein M promotes the anti-inflammatory effect of high-density lipoprotein by binding to scavenger receptor BI.

Background: Inflammation participates pivotally in the pathogenesis of atherosclerosis. Apolipoprotein M (apoM) is a high-density lipoprotein (HDL)-associated plasma protein that affects HDL metabolism and shows various anti-inflammatory functions in atherosclerosis. In this study, we aim to determine whether apoM is expressed in peripheral blood mononuclear cells (PBMCs) and promoted the anti-inflammatory effect of HDL by combing with scavenger receptor BI (SR-BI).

Methods: The expression of apoM in PBMCs is detected by a confocal fluorescence microscope and flow cytometry. The interactions between apoM and SR-BI are detected with co-immunoprecipitation. The multiplexed Luminex xMAP assay detects the inflammatory factors induced by apoM HDL and apoM HDL in inflammatory cell model.

Results: ApoM is expressed on CD14 monocytes, CD3 T cells, and CD19 B cells, CD16 and CD56 NK cells. CD14 monocytes have the highest ratio of apoM cells. ApoM HDL, apoM HDL, and recombinant apoM protein could be co-precipitated with SR-BI on the surface of human THP-1 monocytic leukemia cells. In vitro, apoM HDL induces significantly less expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-1β than apoM HDL.

Conclusions: ApoM was expressed on all PBMCs. ApoM interacted with SR-BI on THP-1. ApoM HDL has a more significant anti-inflammatory effect than apoM HDL.