PUBLICATION
Granulocyte Colony-Stimulating Factor Mediated Regulation of Early Myeloid Cells in Zebrafish
- Authors
- Meier, A.B., Basheer, F., Sertori, R., Laird, M., Liongue, C., Ward, A.C.
- ID
- ZDB-PUB-220427-2
- Date
- 2022
- Source
- Frontiers in bioscience (Landmark edition) 27: 110 (Journal)
- Registered Authors
- Liongue, Clifford
- Keywords
- CSF3, CSF3R, G-CSF, G-CSFR, migration, myelopoiesis, wound healing
- MeSH Terms
-
- Animals
- Granulocyte Colony-Stimulating Factor/genetics
- Janus Kinases/metabolism
- Myeloid Cells
- Phosphatidylinositol 3-Kinases*/metabolism
- Zebrafish*/genetics
- Zebrafish*/metabolism
- PubMed
- 35468669 Full text @ Front Biosci (Landmark Ed)
Citation
Meier, A.B., Basheer, F., Sertori, R., Laird, M., Liongue, C., Ward, A.C. (2022) Granulocyte Colony-Stimulating Factor Mediated Regulation of Early Myeloid Cells in Zebrafish. Frontiers in bioscience (Landmark edition). 27:110.
Abstract
Background Colony-stimulating factor 3 (CSF3), more commonly known as granulocyte colony-stimulating factor (G-CSF), acts via a specific cell surface receptor CSF3R (or G-CSFR) to regulate hematopoiesis, with a particularly key role in the myeloid cell lineage where it impacts the development and function of neutrophilic granulocytes. Zebrafish possess a conserved CSF3R homologue, Csf3r, which is involved in both steady-state and emergency myelopoiesis, as well as regulating early myeloid cell migration. Two CSF3 proteins have been identified in zebrafish, Csf3a and Csf3b.
Methods This study investigated the roles of the Csf3a and Csf3b ligands as well as the downstream Janus kinase (JAK) and phosphatidylinositol 3-kinase (PI3K) pathways in mediating the effects of Csf3r in early myeloid cell development and function using gene knockdown and pharmacologic approaches.
Results This study revealed that both Csf3a and Csf3b contribute to the developmental and emergency production of early myeloid cells, but Csf3a is responsible for the developmental migration of early neutrophils whereas Csf3b plays the major role in their wounding-induced migration, differentially participated in these responses, as did several downstream signaling pathways. Both JAK and PI3K signaling were required for developmental production and migration of early myeloid cells, but PI3K signaling was required for emergency production and initial migration in response to wounding, while JAK signaling mediated retention at the site of wounding.
Conclusions This study has revealed both distinct and overlapping functions for Csf3a and Csf3b and the downstream JAK and PI3K signaling pathways in early myeloid cell production and function.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping