PUBLICATION
NADPH-Oxidase Derived Hydrogen Peroxide and Irs2b Facilitate Re-oxygenation-Induced Catch-Up Growth in Zebrafish Embryo
- Authors
- Zasu, A., Hishima, F., Thauvin, M., Yoneyama, Y., Kitani, Y., Hakuno, F., Volovitch, M., Takahashi, S.I., Vriz, S., Rampon, C., Kamei, H.
- ID
- ZDB-PUB-220720-11
- Date
- 2022
- Source
- Frontiers in endocrinology 13: 929668 (Journal)
- Registered Authors
- Rampon, Christine, Vriz, Sophie
- Keywords
- NADPH-oxidase, catch-up growth, hydrogen peroxide, hypoxia, insulin receptor substrate 2, insulin-like growth factor, re-oxygenation, zebrafish
- MeSH Terms
-
- Animals
- Hydrogen Peroxide
- Hypoxia/metabolism
- Mammals/metabolism
- NADP/metabolism
- NADPH Oxidases/genetics
- NADPH Oxidases/metabolism
- Oxygen/metabolism
- Somatomedins*/metabolism
- Zebrafish*
- PubMed
- 35846271 Full text @ Front Endocrinol (Lausanne)
Citation
Zasu, A., Hishima, F., Thauvin, M., Yoneyama, Y., Kitani, Y., Hakuno, F., Volovitch, M., Takahashi, S.I., Vriz, S., Rampon, C., Kamei, H. (2022) NADPH-Oxidase Derived Hydrogen Peroxide and Irs2b Facilitate Re-oxygenation-Induced Catch-Up Growth in Zebrafish Embryo. Frontiers in endocrinology. 13:929668.
Abstract
Oxygen deprivation induces multiple changes at the cellular and organismal levels, and its re-supply also brings another special physiological status. We have investigated the effects of hypoxia/re-oxygenation on embryonic growth using the zebrafish model: hypoxia slows embryonic growth, but re-oxygenation induces growth spurt or catch-up growth. The mitogen-activated kinase (MAPK)-pathway downstream insulin-like growth factor (IGF/Igf) has been revealed to positively regulate the re-oxygenation-induced catch-up growth, and the role of reactive oxygen species generated by environmental oxygen fluctuation is potentially involved in the phenomenon. Here, we report the role of NADPH-oxidase (Nox)-dependent hydrogen peroxide (H2O2) production in the MAPK-activation and catch-up growth. The inhibition of Nox significantly blunted catch-up growth and MAPK-activity. Amongst two zebrafish insulin receptor substrate 2 genes (irs2a and irs2b), the loss of irs2b, but not its paralog irs2a, resulted in blunted MAPK-activation and catch-up growth. Furthermore, irs2b forcedly expressed in mammalian cells allowed IGF-MAPK augmentation in the presence of H2O2, and the irs2b deficiency completely abolished the somatotropic action of Nox in re-oxygenation condition. These results indicate that redox signaling alters IGF/Igf signaling to facilitate hypoxia/re-oxygenation-induced embryonic growth compensation.
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Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping