Apolipoprotein A1 deficiency in mice primes bone marrow stem cells for T cell lymphopoiesis

Amber B. Ouweneel, Myrthe E. Reiche, Olga S.C. Snip, Robbert Wever, Ezra J. van der Wel, Frank H. Schaftenaar, Soňa Kauerova, Esther Lutgens, Miranda Van Eck, Menno Hoekstra

Research output: Contribution to journalArticlepeer-review


The bone marrow has emerged as a potentially important target in cardiovascular disease as it generates all leukocytes involved in atherogenesis. In the current study, we evaluated whether a change in bone marrow functionality underlies the increased atherosclerosis susceptibility associated with high-density lipoprotein (HDL) deficiency. We found that HDL deficiency in mice due to the genetic lack of hepatocyte-derived apolipoprotein A1 (APOA1) was associated with an increase in the Lin-Sca-1+Kit+ (LSK) bone marrow stem cell population and lymphoid-primed multipotent progenitor numbers, which translated into a higher production and systemic flux of T cell subsets. In accordance with APOA1 deficiencyassociated priming of stem cells to increase T lymphocyte production, atherogenic diet-fed low-density lipoprotein receptor knockout mice transplanted with bone marrow from APOA1-knockout mice displayed marked lymphocytosis as compared to wild-type bone marrow recipients. However, atherosclerotic lesion sizes and collagen contents were similar in the two groups of bone marrow recipients. In conclusion, systemic lack of APOA1 primes bone marrow stem cells for T cell lymphopoiesis. Our data provide novel evidence for a regulatory role of HDL in bone marrow functioning in normolipidemic mice.

Original languageEnglish (US)
Article numberjcs25890
JournalJournal of cell science
Issue number5
StatePublished - Mar 2022


  • Apolipoprotein
  • Bone marrow
  • High-density lipoprotein
  • Lymphopoiesis
  • Stem cells

ASJC Scopus subject areas

  • Cell Biology


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