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.