Hypoxic induction of vascular endothelial growth factor regulates erythropoiesis but not hematopoietic stem cell function in the fetal liver.
Författare
Summary, in English
Hypoxia is an important factor in the hematopoietic stem cell (HSC) niche in the bone marrow, but whether it also plays a role in the regulation of fetal liver (FL) HSCs is unclear. Vascular endothelial growth factor A (VEGFA) is essential for adult HSC survival, and hypoxic induction of VEGFA in adult HSCs is required for proper function. Loss of hypoxia-regulated VEGFA expression increases the number of phenotypically defined hematopoietic stem and progenitor cells in the FL, but whether stem cell function is affected in FL HSCs has not, to our knowledge, been assessed. We show that fetal erythropoiesis is severely impaired when hypoxic induction of VEGFA is lacking. Fetal liver HSCs deficient for hypoxia-induced VEGFA expression have normal HSC function, arguing against a hypoxic FL HSC niche. However, after adaptation of FL HSCs to the bone marrow microenvironment, FL HSCs lose their function, as measured by serial transplantation.
Avdelning/ar
- Avdelningen för molekylärmedicin och genterapi
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Publiceringsår
2014
Språk
Engelska
Sidor
941-944
Publikation/Tidskrift/Serie
Experimental Hematology
Volym
42
Issue
11
Länkar
Dokumenttyp
Artikel i tidskrift
Förlag
Elsevier
Ämne
- Hematology
Status
Published
ISBN/ISSN/Övrigt
- ISSN: 1873-2399