
Vegf regulates embryonic erythroid development through Gata1 modulation
- Author
- Benjamin Drogat (UGent) , Joanna Kalucka, Laura Gutierrez, Hamida Hammad (UGent) , Steven Goossens (UGent) , Morvarid Farhang Ghahremani (UGent) , Sona Bartunkova (UGent) , Katharina Haigh (UGent) , Kim Deswarte (UGent) , Omar Nyabi, Michaël Naessens (UGent) , Napoleone Ferrara, Uursula Klingmuller, Bart Lambrecht (UGent) , Andras Nagy, Sjaak Philipsen and Jody Haigh (UGent)
- Organization
- Abstract
- To determine the role of vascular endothelial growth factor (Vegf) in embryonic erythroid development we have deleted or overexpressed Vegf specifically in the erythroid lineage using the EpoR-iCre transgenic line in combination with Cre/ loxP conditional gain and loss of function Vegf alleles. ROSA26 promoter-based expression of the Vegf164 isoform in the early erythroid lineage resulted in a differentiation block of primitive erythroid progenitor (EryP) development and a partial block in definitive erythropoiesis between the erythroid burst-forming unit and erythroid colony-forming unit stages. Decreased mRNA expression levels of the key erythroid transcription factor Gata1 were causally linked to this phenotype. Conditional deletion of Vegf within the erythroid lineage was associated with increased Gata1 levels and increased erythroid differentiation. Expression of a ROSA26-based GATA2 transgene rescued Gata1 mRNAlevels and target genes and restored erythroid differentiation in our Vegf gain of function model. These results demonstrate that Vegf modulates Gata1 expression levels in vivo and provides new molecular insight into Vegf’s ability to modulate erythropoiesis.
- Keywords
- HEMATOPOIETIC STEM-CELLS, DEFINITIVE HEMATOPOIESIS, TRANSCRIPTION FACTOR GATA-1, GENE-EXPRESSION, YOLK-SAC, MOUSE, DIFFERENTIATION, ERYTHROPOIETIN, SURVIVAL, LINEAGE
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Citation
Please use this url to cite or link to this publication: http://hdl.handle.net/1854/LU-1060090
- MLA
- Drogat, Benjamin, et al. “Vegf Regulates Embryonic Erythroid Development through Gata1 Modulation.” BLOOD, vol. 116, no. 12, 2010, pp. 2141–51, doi:10.1182/blood-2010-01-264143.
- APA
- Drogat, B., Kalucka, J., Gutierrez, L., Hammad, H., Goossens, S., Farhang Ghahremani, M., … Haigh, J. (2010). Vegf regulates embryonic erythroid development through Gata1 modulation. BLOOD, 116(12), 2141–2151. https://doi.org/10.1182/blood-2010-01-264143
- Chicago author-date
- Drogat, Benjamin, Joanna Kalucka, Laura Gutierrez, Hamida Hammad, Steven Goossens, Morvarid Farhang Ghahremani, Sona Bartunkova, et al. 2010. “Vegf Regulates Embryonic Erythroid Development through Gata1 Modulation.” BLOOD 116 (12): 2141–51. https://doi.org/10.1182/blood-2010-01-264143.
- Chicago author-date (all authors)
- Drogat, Benjamin, Joanna Kalucka, Laura Gutierrez, Hamida Hammad, Steven Goossens, Morvarid Farhang Ghahremani, Sona Bartunkova, Katharina Haigh, Kim Deswarte, Omar Nyabi, Michaël Naessens, Napoleone Ferrara, Uursula Klingmuller, Bart Lambrecht, Andras Nagy, Sjaak Philipsen, and Jody Haigh. 2010. “Vegf Regulates Embryonic Erythroid Development through Gata1 Modulation.” BLOOD 116 (12): 2141–2151. doi:10.1182/blood-2010-01-264143.
- Vancouver
- 1.Drogat B, Kalucka J, Gutierrez L, Hammad H, Goossens S, Farhang Ghahremani M, et al. Vegf regulates embryonic erythroid development through Gata1 modulation. BLOOD. 2010;116(12):2141–51.
- IEEE
- [1]B. Drogat et al., “Vegf regulates embryonic erythroid development through Gata1 modulation,” BLOOD, vol. 116, no. 12, pp. 2141–2151, 2010.
@article{1060090, abstract = {{To determine the role of vascular endothelial growth factor (Vegf) in embryonic erythroid development we have deleted or overexpressed Vegf specifically in the erythroid lineage using the EpoR-iCre transgenic line in combination with Cre/ loxP conditional gain and loss of function Vegf alleles. ROSA26 promoter-based expression of the Vegf164 isoform in the early erythroid lineage resulted in a differentiation block of primitive erythroid progenitor (EryP) development and a partial block in definitive erythropoiesis between the erythroid burst-forming unit and erythroid colony-forming unit stages. Decreased mRNA expression levels of the key erythroid transcription factor Gata1 were causally linked to this phenotype. Conditional deletion of Vegf within the erythroid lineage was associated with increased Gata1 levels and increased erythroid differentiation. Expression of a ROSA26-based GATA2 transgene rescued Gata1 mRNAlevels and target genes and restored erythroid differentiation in our Vegf gain of function model. These results demonstrate that Vegf modulates Gata1 expression levels in vivo and provides new molecular insight into Vegf’s ability to modulate erythropoiesis.}}, author = {{Drogat, Benjamin and Kalucka, Joanna and Gutierrez, Laura and Hammad, Hamida and Goossens, Steven and Farhang Ghahremani, Morvarid and Bartunkova, Sona and Haigh, Katharina and Deswarte, Kim and Nyabi, Omar and Naessens, Michaël and Ferrara, Napoleone and Klingmuller, Uursula and Lambrecht, Bart and Nagy, Andras and Philipsen, Sjaak and Haigh, Jody}}, issn = {{0006-4971}}, journal = {{BLOOD}}, keywords = {{HEMATOPOIETIC STEM-CELLS,DEFINITIVE HEMATOPOIESIS,TRANSCRIPTION FACTOR GATA-1,GENE-EXPRESSION,YOLK-SAC,MOUSE,DIFFERENTIATION,ERYTHROPOIETIN,SURVIVAL,LINEAGE}}, language = {{eng}}, number = {{12}}, pages = {{2141--2151}}, title = {{Vegf regulates embryonic erythroid development through Gata1 modulation}}, url = {{http://dx.doi.org/10.1182/blood-2010-01-264143}}, volume = {{116}}, year = {{2010}}, }
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