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

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023001%3A_____%2F22%3A00082532" target="_blank" >RIV/00023001:_____/22:00082532 - isvavai.cz</a>

Výsledek na webu

<a href="https://journals.biologists.com/jcs/article/135/5/jcs258901/273436/Apolipoprotein-A1-deficiency-in-mice-primes-bone" target="_blank" >https://journals.biologists.com/jcs/article/135/5/jcs258901/273436/Apolipoprotein-A1-deficiency-in-mice-primes-bone</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1242/jcs.258901" target="_blank" >10.1242/jcs.258901</a>

Jazyk výsledku

angličtina

Název v původním jazyce

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

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

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

Popis výsledku anglicky

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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10601 - Cell biology

Projekt

—

Návaznosti

V - Vyzkumna aktivita podporovana z jinych verejnych zdroju

Rok uplatnění

2022

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of cell science

ISSN

0021-9533

e-ISSN

1477-9137

Svazek periodika

135

Číslo periodika v rámci svazku

5

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

9

Strana od-do

"Art. no. jcs258901"

Kód UT WoS článku

000783839400020

EID výsledku v databázi Scopus

2-s2.0-85121958430