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Apolipoprotein A1 deficiency in mice primes bone marrow stem cells for T cell lymphopoiesis
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 hi...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Company of Biologists Ltd
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8645231/ https://www.ncbi.nlm.nih.gov/pubmed/34698355 http://dx.doi.org/10.1242/jcs.258901 |
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author | Ouweneel, Amber B. Reiche, Myrthe E. Snip, Olga S. C. Wever, Robbert van der Wel, Ezra J. Schaftenaar, Frank H. Kauerova, Soňa Lutgens, Esther Van Eck, Miranda Hoekstra, Menno |
author_facet | Ouweneel, Amber B. Reiche, Myrthe E. Snip, Olga S. C. Wever, Robbert van der Wel, Ezra J. Schaftenaar, Frank H. Kauerova, Soňa Lutgens, Esther Van Eck, Miranda Hoekstra, Menno |
author_sort | Ouweneel, Amber B. |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-8645231 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | The Company of Biologists Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-86452312021-12-10 Apolipoprotein A1 deficiency in mice primes bone marrow stem cells for T cell lymphopoiesis Ouweneel, Amber B. Reiche, Myrthe E. Snip, Olga S. C. Wever, Robbert van der Wel, Ezra J. Schaftenaar, Frank H. Kauerova, Soňa Lutgens, Esther Van Eck, Miranda Hoekstra, Menno J Cell Sci Research Article 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. The Company of Biologists Ltd 2021-11-16 /pmc/articles/PMC8645231/ /pubmed/34698355 http://dx.doi.org/10.1242/jcs.258901 Text en © 2021. Published by The Company of Biologists Ltd https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed. |
spellingShingle | Research Article Ouweneel, Amber B. Reiche, Myrthe E. Snip, Olga S. C. Wever, Robbert van der Wel, Ezra J. Schaftenaar, Frank H. Kauerova, Soňa Lutgens, Esther Van Eck, Miranda Hoekstra, Menno Apolipoprotein A1 deficiency in mice primes bone marrow stem cells for T cell lymphopoiesis |
title | Apolipoprotein A1 deficiency in mice primes bone marrow stem cells for T cell lymphopoiesis |
title_full | Apolipoprotein A1 deficiency in mice primes bone marrow stem cells for T cell lymphopoiesis |
title_fullStr | Apolipoprotein A1 deficiency in mice primes bone marrow stem cells for T cell lymphopoiesis |
title_full_unstemmed | Apolipoprotein A1 deficiency in mice primes bone marrow stem cells for T cell lymphopoiesis |
title_short | Apolipoprotein A1 deficiency in mice primes bone marrow stem cells for T cell lymphopoiesis |
title_sort | apolipoprotein a1 deficiency in mice primes bone marrow stem cells for t cell lymphopoiesis |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8645231/ https://www.ncbi.nlm.nih.gov/pubmed/34698355 http://dx.doi.org/10.1242/jcs.258901 |
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