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T. Suzuki et al.
increased trafficking of HPC from the BM cavity into the circulation. In addition to the consequences of using dif- ferent models, proteolytic processing and post-translation- al modifications of Angptl4 may occur differently in each organ and each type of producer and effector cell, resulting in widely variable results.
BM is tightly regulated by the SNS, and a major step for
HSPC mobilization by G-CSF is the strong suppression of
tion (Figure 7D). Our study has shed light on oral fat as an important regulator of interorgan communication between the nervous and hematopoietic systems.
Disclosures
No conflicts of interest to disclose.
Contributions
TS performed all the experiments and wrote the manuscript; SI, YKaw, KW, HK, AS, and KM helped with animal mainte- nance and tissue sample preparation; MS and TF performed the bone marrow lipid analysis; MH and ST supervised the study of PPARd-deficient mice; NST supervised the study with anti- Angptl4 antibody; TM supervised all experiments; and YKat supervised all experiments and wrote the manuscript.
Funding
This work was supported by PRESTO, the Japan Science and Technology Agency (#JPMJPR12M7; to YKat), CREST grant from AMED (#JP18gm0910012h2; to YKat), and Grants-in- Aid for Scientific Research (#15H04856 and #18H02837; to YKat) from the Japan Society for the Promotion of Science.
osteolineage cells, such as osteoblasts and osteocytes, via
b -AR stimulation by catecholamines.7-9 G-CSF stimula- 2
tion of sympathetic nerves inhibits the reuptake of
released catecholamines at the synapse,10 leading to hyper-
sympathetic tone in the BM. We have previously shown
that BM neutrophils express all b -, b -, and b -AR and that 123
the selective b -AR agonist activates the arachidonic acid 3
cascade to increase PGE production to protect osteoblast
2
function. In this study, induction of PPARd mRNA and
11
protein by SNS signals was mainly through b /b -AR in 12
mature/immature neutrophils. The b /b -AR-PPARd/ω3- 12
PUFA-Angptl4 pathway in BM myeloid cells counteracts the alteration of the BM microenvironment and suppress- es mobilization upon G-CSF-induced marrow inflamma-
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