| First Author | Berger A | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 3 | Pages | e58787 |
| PubMed ID | 23516556 | Mgi Jnum | J:199916 |
| Mgi Id | MGI:5505764 | Doi | 10.1371/journal.pone.0058787 |
| Citation | Berger A, et al. (2013) Neurokinin-1 receptor signalling impacts bone marrow repopulation efficiency. PLoS One 8(3):e58787 |
| abstractText | Tachykinins are a large group of neuropeptides with both central and peripheral activity. Despite the increasing number of studies reporting a growth supportive effect of tachykinin peptides in various in vitro stem cell systems, it remains unclear whether these findings are applicable in vivo. To determine how neurokinin-1 receptor (NK-1R) deficient hematopoietic stem cells would behave in a normal in vivo environment, we tested their reconstitution efficiency using competitive bone marrow repopulation assays. We show here that bone marrow taken from NK-1R deficient mice (Tacr1(-/-)) showed lineage specific B and T cell engraftment deficits compared to wild-type competitor bone marrow cells, providing evidence for an involvement of NK-1R signalling in adult hematopoiesis. Tachykinin knockout mice lacking the peptides SP and/or HK-1 (Tac1 (-/-), Tac4 (-/-) and Tac1 (-/-)/Tac4 (-/-) mice) repopulated a lethally irradiated wild-type host with similar efficiency as competing wild-type bone marrow. The difference between peptide and receptor deficient mice indicates a paracrine and/or endocrine mechanism of action rather than autocrine signalling, as tachykinin peptides are supplied by the host environment. |
