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.