PUBLICATION
Zebrafish Heme Oxygenase 1a Is Necessary for Normal Development and Macrophage Migration
- Authors
- Luo, K., Ogawa, M., Ayer, A., Britton, W.J., Stocker, R., Kikuchi, K., Oehlers, S.H.
- ID
- ZDB-PUB-220203-9
- Date
- 2022
- Source
- Zebrafish 19(1): 7-17 (Journal)
- Registered Authors
- Kikuchi, Kazu, Luo, Kaiming, Oehlers, Stefan, Ogawa, Mashahito
- Keywords
- HMOX, heme oxygenase, macrophage
- MeSH Terms
-
- Animals
- Heme Oxygenase (Decyclizing)*/metabolism
- Heme Oxygenase (Decyclizing)*/pharmacology
- Macrophages/metabolism
- Mice
- Oxidative Stress
- Zebrafish*/metabolism
- PubMed
- 35108124 Full text @ Zebrafish
Citation
Luo, K., Ogawa, M., Ayer, A., Britton, W.J., Stocker, R., Kikuchi, K., Oehlers, S.H. (2022) Zebrafish Heme Oxygenase 1a Is Necessary for Normal Development and Macrophage Migration. Zebrafish. 19(1):7-17.
Abstract
Heme oxygenase function is highly conserved between vertebrates where it plays important roles in normal embryonic development and controls oxidative stress. Expression of the zebrafish heme oxygenase 1 genes is known to be responsive to oxidative stress suggesting a conserved physiological function. In this study, we generate a knockout allele of zebrafish hmox1a and characterize the effects of hmox1a and hmox1b loss on embryonic development. We find that loss of hmox1a or hmox1b causes developmental defects in only a minority of embryos, in contrast to Hmox1 gene deletions in mice that cause loss of most embryos. Using a tail wound inflammation assay we find a conserved role for hmox1a, but not hmox1b, in normal macrophage migration to the wound site. Together our results indicate that zebrafish hmox1a has clearly a partitioned role from hmox1b that is more consistent with conserved functions of mammalian Heme oxygenase 1.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping