Fetal liver hematopoietic stem cell niches associate with portal vessels

Author:

Khan Jalal A.123,Mendelson Avital12,Kunisaki Yuya12,Birbrair Alexander12,Kou Yan4,Arnal-Estapé Anna12,Pinho Sandra12,Ciero Paul1,Nakahara Fumio12,Ma’ayan Avi4,Bergman Aviv5,Merad Miriam3,Frenette Paul S.126

Affiliation:

1. Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research. Albert Einstein College of Medicine, Bronx, NY, USA.

2. Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY, USA.

3. Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

4. Department of Pharmacology and Systems Therapeutics, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

5. Department of Systems and Computational Biology, Albert Einstein College of Medicine, Bronx, NY, USA.

6. Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, USA.

Abstract

How HSCs populate the fetal liver Hematopoietic stem cells (HSCs) undergo dramatic expansion in the fetal liver before migrating to their definitive site in the bone marrow. Khan et al. identify portal vessel–associated Nestin + NG2 + pericytes as critical HSC niche components (see the Perspective by Cabezas-Wallscheid and Trumpp). The portal vessel niche and HSCs expand according to fractal geometries, suggesting that niche cells—rather than factors expressed by the niche—drive HSC proliferation. After birth, arterial portal vessels transform into portal veins, and lose Nestin + NG2 + pericytes. When this happens, the niche is lost and HSCs migrate away from the neonatal liver. Science , this issue p. 176 ; see also p. 126

Funder

NIH

NYSTEM

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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