Hypoxic induction of vascular endothelial growth factor regulates erythropoiesis but not hematopoietic stem cell function in the fetal liver.
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/4691540
- author
- Rehn, Matilda LU ; Kertész, Zsuzsanna LU and Cammenga, Jörg LU
- organization
- publishing date
- 2014
- 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
- pmid:25220588
- 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
- 2016-04-01 09:55:11
- date last changed
- 2022-02-02 04:42:03
@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}}, doi = {{10.1016/j.exphem.2014.08.002}}, volume = {{42}}, year = {{2014}}, }