Abstract
Glutathione peroxidase 1 (Gpx1) and peroxiredoxin 2 (Prdx2) belong to the thiol peroxidase family of antioxidants, and have been studied for their antioxidant functions and roles in cancers. However, the physiological significance of Gpx1 and Prdx2 during vertebrate embryogenesis are lacking. Currently, we investigated the functional roles of Gpx1 and Prdx2 during vertebrate embryogenesis using Xenopus laevis as a vertebrate model. Our investigations revealed the zygotic nature of gpx1 having its localization in the eye region of developing embryos, whereas prdx2 exhibited a maternal nature and were localized in embryonic ventral blood islands. Furthermore, the gpx1-morphants exhibited malformed eyes with incompletely detached lenses. However, the depletion of prdx2 has not established its involvement with embryogenesis. A molecular analysis of gpx1-depleted embryos revealed the perturbed expression of a cryba1-lens-specific marker and also exhibited reactive oxygen species (ROS) accumulation in the eye regions of gpx1-morphants. Additionally, transcriptomics analysis of gpx1-knockout embryos demonstrated the involvement of Wnt, cadherin, and integrin signaling pathways in the development of malformed eyes. Conclusively, our findings indicate the association of gpx1 with a complex network of embryonic developmental pathways and ROS responses, but detailed investigation is a prerequisite in order to pinpoint the mechanistic details of these interactions.
Highlights
IntroductionAerobic metabolism results in cellular energy production along with the generation of a toxic oxygen intermediate termed “reactive oxygen species” (ROS), which in excess amounts causes cellular homeostasis disturbance [1]
St. 30 of embryogenesis made us speculate about the involvement of gpx1 in eye development during Xenopus embryogenesis because optic vesicle formation starts at the NF
We conducted a Whole-Mount In Situ Hybridization (WISH) analysis to determine the spatial expression of gpx1 during Xenopus embryogenesis
Summary
Aerobic metabolism results in cellular energy production along with the generation of a toxic oxygen intermediate termed “reactive oxygen species” (ROS), which in excess amounts causes cellular homeostasis disturbance [1]. Among the different ROS, peroxides (e.g., H2 O2 ) are generated by a diverse variety of metabolic processes, such as superoxide anion dismutation, or as oxidase byproducts [2]. Organic peroxides are produced in the cells by cyclooxygenase and lipoxygenase actions or due to polyunsaturated fatty acid oxidation [2]. ROS are important signaling molecules at physiological or low levels in the cells, activating/deactivating important signaling pathways [3], and they play significant roles in embryonic development [4]. Excess amounts of ROS damage cells, and Antioxidants 2021, 10, 1636.
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