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Gamrekelashvili, J.* ; Giagnorio, R.* ; Jussofie, J.* ; Soehnlein, O.* ; Duchene, J.* ; Briseño, C.G.* ; Ramasamy, S.K.* ; Krishnasamy, K.* ; Limbourg, A.* ; Kapanadze, T.* ; Ishifune, C.* ; Hinkel, R.* ; Radtke, F.* ; Strobl, L.J. ; Zimber-Strobl, U. ; Napp, L.C.* ; Bauersachs, J.* ; Haller, H.* ; Yasutomo, K.* ; Kupatt, C.* ; Murphy, K.M.* ; Adams, R.H.* ; Weber, C.* ; Limbourg, F.P.*

Regulation of monocyte cell fate by blood vessels mediated by Notch signalling.

Nat. Commun. 7:12597 (2016)
Publ. Version/Full Text Supplement DOI PMC
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A population of monocytes, known as Ly6C(lo) monocytes, patrol blood vessels by crawling along the vascular endothelium. Here we show that endothelial cells control their origin through Notch signalling. Using combinations of conditional genetic deletion strategies and cell-fate tracking experiments we show that Notch2 regulates conversion of Ly6C(hi) monocytes into Ly6C(lo) monocytes in vivo and in vitro, thereby regulating monocyte cell fate under steady-state conditions. This process is controlled by Notch ligand delta-like 1 (Dll1) expressed by a population of endothelial cells that constitute distinct vascular niches in the bone marrow and spleen in vivo, while culture on recombinant DLL1 induces monocyte conversion in vitro. Thus, blood vessels regulate monocyte conversion, a form of committed myeloid cell fate regulation.
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Publication type Article: Journal article
Document type Scientific Article
Keywords Hematopoietic Stem-cells; Green Fluorescent Protein; Dendritic Cells; Postnatal Arteriogenesis; Classical Monocytes; Lineage Commitment; Angiocrine Factors; Endothelial-cells; Vascular Niche; Lymph-nodes
Language english
Publication Year 2016
HGF-reported in Year 2016
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Quellenangaben Volume: 7, Issue: , Pages: , Article Number: 12597 Supplement: ,
Publisher Nature Publishing Group
Publishing Place London
Reviewing status Peer reviewed
POF-Topic(s) 30203 - Molecular Targets and Therapies
Research field(s) Immune Response and Infection
PSP Element(s) G-501500-003
PubMed ID 27576369
Scopus ID 84984985562
Erfassungsdatum 2016-09-02