Journal
BLOOD ADVANCES
Volume 5, Issue 6, Pages 1594-1604Publisher
ELSEVIER
DOI: 10.1182/bloodadvances.2020002410
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Funding
- Japan Society for the Promotion of Science (JSPS) [17K16191]
- JSPS [19J00952, 19H03688, 19K22641, 26221309]
- Uehara Memorial Foundation
- Singapore Ministry of Health's National Medical Research Council under NMRC/MOH-STaR18May [MOH-000149]
- Grants-in-Aid for Scientific Research [26221309, 17K16191, 19J00952, 19H03688, 19K22641] Funding Source: KAKEN
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The role of autophagy in neonatal HSCs is unclear, but it has an impact on the regulation of adult HSCs.
Hematopoietic stem cells (HSCs) undergo self-renewal or differentiation to sustain lifelong hematopoiesis. HSCs are preserved in quiescence with low mitochondrial activity. Recent studies indicate that autophagy contributes to HSC quiescence through suppressing mitochondrial metabolism. However, it remains unclear whether autophagy is involved in the regulation of neonatal HSCs, which proliferate actively. In this study, we clarified the role of autophagy in neonatal HSCs using 2 types of autophagy-related gene 7 (Atg7)-conditional knockout mice: Mx1-Cre inducible system and Vav-Cre system. Atg7-deficient HSCs exhibited excess cell divisions with enhanced mitochondrial metabolism, leading to bone marrow failure at adult stage. However, Atg7 deficiency minimally affected hematopoiesis and metabolic state in HSCs at neonatal stage. In addition, Atg7-deficient neonatal HSCs exhibited long-term reconstructing activity, equivalent to wild-type neonatal HSCs. Taken together, autophagy is dispensable for stem cell function and hematopoietic homeostasis in neonates and provide a novel aspect into the role of autophagy in the HSC regulation.
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