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Hepatic Apolipoprotein M Suppresses Hepatocyte Secretion of Prothrombin by Upregulating Arid5B

Makoto Kurano1, Baasanjav Uranbileg1, Yutaka Yatomi1

  • 1Department of Clinical Laboratory Medicine, The University of Tokyo, Tokyo, Japan.

Thrombosis and Haemostasis
|July 28, 2025
PubMed
Abstract

Insights

Apolipoprotein M (ApoM) influences blood clotting by regulating prothrombin levels. ApoM suppresses prothrombin secretion from hepatocytes, impacting platelet counts and coagulation times.

Area of Science:

  • Biochemistry
  • Hematology
  • Molecular Biology

Background:

  • High-density lipoprotein (HDL) exhibits pleiotropic effects, including anti-thrombotic properties.
  • Apolipoprotein M (ApoM), an HDL-associated protein, carries sphingosine-1-phosphate (S1P).
  • The role of ApoM in coagulopathy remains largely unexplored.

Purpose of the Study:

  • To investigate the association between Apolipoprotein M (ApoM) and coagulopathy.
  • To elucidate the mechanisms by which ApoM affects coagulation parameters.

Main Methods:

  • Murine lipopolysaccharide-induced sepsis model to assess coagulopathy.
  • ApoM overexpression and knockout mouse models.
  • Prothrombin time and activated partial thromboplastin time assays.
  • HepG2 cell line experiments for prothrombin secretion analysis.
  • RNA sequencing to identify interacting factors.

Main Results:

  • ApoM modulated platelet counts and coagulation times in a sepsis model.
  • ApoM decreased plasma prothrombin levels while increasing hepatic and cellular prothrombin levels.
  • ApoM upregulated Arid5B expression in hepatocytes.
  • Arid5B knockdown antagonized ApoM's inhibitory effect on prothrombin secretion, independent of S1P receptors.

Conclusions:

  • Hepatic ApoM suppresses hepatocyte prothrombin secretion via Arid5B upregulation.
  • ApoM plays a significant role in regulating coagulopathy, independent of S1P signaling pathways.

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