PUBLICATION
Vascular endothelial growth factor-c regulates hematopoietic stem cell fate in the dorsal aorta
- Authors
- Schiavo, R.K., Tamplin, O.J.
- ID
- ZDB-PUB-211221-12
- Date
- 2021
- Source
- Development (Cambridge, England) 149(2): (Journal)
- Registered Authors
- Tamplin, Owen
- Keywords
- Dorsal aorta, Hematopoiesis, Hematopoietic stem cells, Hemogenic endothelium, VEGFC, Zebrafish
- Datasets
- GEO:GSE186565
- MeSH Terms
-
- Animals
- Aorta/cytology*
- Aorta/embryology
- Cell Differentiation*
- Cells, Cultured
- Endothelium, Vascular/cytology
- Endothelium, Vascular/embryology
- Hematopoietic Stem Cells/cytology
- Hematopoietic Stem Cells/metabolism*
- Loss of Function Mutation
- Myeloid Cells/cytology
- Myeloid Cells/metabolism
- Vascular Endothelial Growth Factor C/genetics
- Vascular Endothelial Growth Factor C/metabolism*
- Zebrafish
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 34919128 Full text @ Development
Citation
Schiavo, R.K., Tamplin, O.J. (2021) Vascular endothelial growth factor-c regulates hematopoietic stem cell fate in the dorsal aorta. Development (Cambridge, England). 149(2):.
Abstract
Hematopoietic stem and progenitor cells (HSPCs) are multipotent cells that self-renew or differentiate to establish the entire blood hierarchy. HSPCs arise from the hemogenic endothelium of the dorsal aorta (DA) during development in a process called endothelial-to-hematopoietic transition. The factors and signals that control HSPC fate decisions from the hemogenic endothelium are not fully understood. We found that vegfc has a role in HSPC emergence from the zebrafish DA. Using time-lapse live imaging, we show that some HSPCs in the DA of vegfc loss-of-function embryos display altered cellular behavior. Instead of typical budding from the DA, emergent HSPCs exhibit crawling behavior similar to myeloid cells. This was confirmed by increased myeloid cell marker expression in the ventral wall of the DA and the caudal hematopoietic tissue. This increase in myeloid cells corresponded with a decrease in HSPCs that persisted into larval stages. Together, our data suggests vegfc regulates HSPC emergence in the hemogenic endothelium, in part by suppressing a myeloid cell fate. Our study provides a potential signal for modulation of HSPC fate in stem cell differentiation protocols.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping