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Semin Cell Dev Biol. 2018 Aug;80:17-28. doi: 10.1016/j.semcdb.2017.09.019. Epub 2017 Sep 22.

Redox stress and signaling during vertebrate embryonic development: Regulation and responses.

Author information

1
Department of Environmental Health Sciences, School of Public Health and Health Sciences, University of Massachusetts, Amherst, MA 01003, USA. Electronic address: aliciat@umass.edu.
2
Biology Department, Woods Hole Oceanographic Institution, Woods Hole, MA 02543, USA.
3
Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USA.
4
Molecular & Cellular Biology Graduate Program, University of Massachusetts, Amherst, MA 01003, USA.
5
Department of Environmental Health Sciences, School of Public Health and Health Sciences, University of Massachusetts, Amherst, MA 01003, USA; Biotechnology Training Program, University of Massachusetts, Amherst, MA 01003, USA.

Abstract

Vertebrate embryonic development requires specific signaling events that regulate cell proliferation and differentiation to occur at the correct place and the correct time in order to build a healthy embryo. Signaling pathways are sensitive to perturbations of the endogenous redox state, and are also susceptible to modulation by reactive species and antioxidant defenses, contributing to a spectrum of passive vs. active effects that can affect redox signaling and redox stress. Here we take a multi-level, integrative approach to discuss the importance of redox status for vertebrate developmental signaling pathways and cell fate decisions, with a focus on glutathione/glutathione disulfide, thioredoxin, and cysteine/cystine redox potentials and the implications for protein function in development. We present a tissue-specific example of the important role that reactive species play in pancreatic development and metabolic regulation. We discuss NFE2L2 (also known as NRF2) and related proteins, their roles in redox signaling, and their regulation of glutathione during development. Finally, we provide examples of xenobiotic compounds that disrupt redox signaling in the context of vertebrate embryonic development. Collectively, this review provides a systems-level perspective on the innate and inducible antioxidant defenses, as well as their roles in maintaining redox balance during chemical exposures that occur in critical windows of development.

KEYWORDS:

Glutathione; Nrf2; Pancreas; Redox proteomics; Toxicology

PMID:
28927759
PMCID:
PMC5650060
[Available on 2019-08-01]
DOI:
10.1016/j.semcdb.2017.09.019

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