Zebrafish <i>Heme Oxygenase 1a</i> Is Necessary for Normal Development and Macrophage Migration
Zebrafish <i>Heme Oxygenase 1a</i> Is Necessary for Normal Development and Macrophage Migration
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斑马鱼<i>血红素加氧酶1a</i>对于正常发育和巨噬细胞迁移是必需的
DOI：
10.1089/zeb.2021.0058
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发表时间：
2022
期刊：
影响因子：
2
通讯作者：
Oehlers Stefan H.
中科院分区：
文献类型：
--
作者：
Luo Kaiming;Ogawa Masahito;Ayer Anita;Britton Warwick J.;Stocker Roland;Kikuchi Kazu;Oehlers Stefan H.
在脊椎动物中，血红素加氧酶的功能高度保守，在正常的胚胎发育和控制氧化应激中发挥着重要作用。斑马鱼的血红素加氧酶1基因的表达是已知的对氧化应激的响应，这表明了一种保守的生理功能。在这项研究中，我们产生了斑马鱼hmox1a的敲除等位基因，并表征了hmox1a和hmox1bloss对胚胎发育的影响。我们发现，hmox1orhmox1b的缺失只会导致少数胚胎的发育缺陷，而小鼠的hmox1基因缺失会导致大多数胚胎的丧失。利用尾部伤口炎症试验，我们发现hmox1a在正常巨噬细胞迁移到伤口部位的过程中起保守作用，而不是hmox1b。综上所述，我们的结果表明斑马鱼hmox1a与hmox1b具有明显的分离作用，这与哺乳动物血红素加氧酶1的保守功能更一致。
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 zebrafishhmox1aand characterize the effects ofhmox1aandhmox1bloss on embryonic development. We find that loss ofhmox1aorhmox1bcauses developmental defects in only a minority of embryos, in contrast toHmox1gene deletions in mice that cause loss of most embryos. Using a tail wound inflammation assay we find a conserved role forhmox1a, but nothmox1b, in normal macrophage migration to the wound site. Together our results indicate that zebrafishhmox1ahas clearly a partitioned role fromhmox1bthat is more consistent with conserved functions of mammalian Heme oxygenase 1.