Apolipoprotein A1 deficiency in mice primes bone marrow stem cells for T cell lymphopoiesis.
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ABSTRACT: 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 deficiency-associated priming of stem cells to increase T lymphocyte production, atherogenic diet-fed
SUBMITTER: Ouweneel AB
PROVIDER: S-EPMC8645231 | biostudies-literature | 2022 Mar
REPOSITORIES: biostudies-literature
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