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Hypoxic induction of vascular endothelial growth factor regulates erythropoiesis but not hematopoietic stem cell function in the fetal liver.

Rehn, Matilda LU ; Kertész, Zsuzsanna LU and Cammenga, Jörg LU (2014) In Experimental Hematology 42(11). p.941-944
Abstract
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... (More)
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. (Less)
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author
organization
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type
Contribution to journal
publication status
published
subject
in
Experimental Hematology
volume
42
issue
11
pages
941 - 944
publisher
Elsevier
external identifiers
  • pmid:25220588
  • wos:000345545300003
  • scopus:84912070119
ISSN
1873-2399
DOI
10.1016/j.exphem.2014.08.002
language
English
LU publication?
yes
id
26028173-13fc-47c9-bbf8-b499b6fff97c (old id 4691540)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/25220588?dopt=Abstract
date added to LUP
2014-10-07 17:20:16
date last changed
2017-10-22 03:02:34
@article{26028173-13fc-47c9-bbf8-b499b6fff97c,
  abstract     = {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.},
  author       = {Rehn, Matilda and Kertész, Zsuzsanna and Cammenga, Jörg},
  issn         = {1873-2399},
  language     = {eng},
  number       = {11},
  pages        = {941--944},
  publisher    = {Elsevier},
  series       = {Experimental Hematology},
  title        = {Hypoxic induction of vascular endothelial growth factor regulates erythropoiesis but not hematopoietic stem cell function in the fetal liver.},
  url          = {http://dx.doi.org/10.1016/j.exphem.2014.08.002},
  volume       = {42},
  year         = {2014},
}