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

Autor:	Ouweneel AB; Division of BioTherapeutics, Leiden Academic Centre for Drug Research, Leiden University, 2333CC Leiden, The Netherlands., Reiche ME; Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Centers, University of Amsterdam, 1105AZ Amsterdam, The Netherlands., Snip OSC; Division of BioTherapeutics, Leiden Academic Centre for Drug Research, Leiden University, 2333CC Leiden, The Netherlands., Wever R; Division of BioTherapeutics, Leiden Academic Centre for Drug Research, Leiden University, 2333CC Leiden, The Netherlands., van der Wel EJ; Division of BioTherapeutics, Leiden Academic Centre for Drug Research, Leiden University, 2333CC Leiden, The Netherlands., Schaftenaar FH; Division of BioTherapeutics, Leiden Academic Centre for Drug Research, Leiden University, 2333CC Leiden, The Netherlands., Kauerova S; Laboratory for Atherosclerosis Research, Institute for Clinical and Experimental Medicine, 12111 Prague, Czech Republic., Lutgens E; Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Centers, University of Amsterdam, 1105AZ Amsterdam, The Netherlands., Van Eck M; Division of BioTherapeutics, Leiden Academic Centre for Drug Research, Leiden University, 2333CC Leiden, The Netherlands., Hoekstra M; Division of BioTherapeutics, Leiden Academic Centre for Drug Research, Leiden University, 2333CC Leiden, The Netherlands.
Jazyk:	angličtina
Zdroj:	Journal of cell science [J Cell Sci] 2022 Mar 01; Vol. 135 (5). Date of Electronic Publication: 2021 Nov 16.
DOI:	10.1242/jcs.258901
Abstrakt:	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 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. Competing Interests: Competing interests The authors declare no competing or financial interests. (© 2021. Published by The Company of Biologists Ltd.)
Databáze:	MEDLINE
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