| Literature DB >> 35108124 |
Kaiming Luo1,2, Masahito Ogawa2, Anita Ayer2,3, Warwick J Britton1,4, Roland Stocker2,3, Kazu Kikuchi2,5, Stefan H Oehlers1,6.
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.Entities:
Keywords: HMOX; heme oxygenase; macrophage
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Year: 2022 PMID: 35108124 DOI: 10.1089/zeb.2021.0058
Source DB: PubMed Journal: Zebrafish ISSN: 1545-8547 Impact factor: 1.985