scholarly journals Elevated and sustained reactive oxygen species levels facilitate mesoderm formation during early Xenopus development

2017 ◽  
Author(s):  
Yue Han ◽  
Yaoyao Chen ◽  
Nick R. Love ◽  
Shoko Ishibashi ◽  
Enrique Amaya
Keyword(s):  
Reactive Oxygen Species ◽  
Growth Factor ◽  
Embryonic Development ◽  
Fluorescent Protein ◽  
Reactive Oxygen ◽  
Signalling Pathways ◽  
Mesoderm Induction ◽  
Oxygen Species ◽  
Mesoderm Formation ◽  
Growth Factor Signalling

ABSTRACTFertilisation triggers embryonic development culminating with the activation of a number of highly co-ordinated and evolutionarily conserved signalling pathways, which induce and pattern the mesoderm of the developing embryo. Previous studies in invertebrates have shown that hydrogen peroxide (H2O2), a reactive oxygen species (ROS), can act as a signalling molecule for axis specification during early development. Using a HyPer transgenic Xenopus laevis line that expresses a H2O2-sensitive fluorescent protein sensor maternally, we recently found that fertilisation triggers a rapid increase in ROS production. Here we show that this increase in ROS levels is sustained throughout early embryogenesis, lasting until the tailbud stages. In addition we show that lowering ROS levels from the blastula stage through the gastrula stages via antioxidant treatments disrupts mesoderm formation. Furthermore, we show that attenuating ROS levels during the blastula / gastrula stages affects some, but not all, growth factor signalling pathways involved in mesoderm induction and patterning, including the PI3K/Akt, TGF-β/Nodal, and Wnt/β-catenin signalling pathways. These data suggest that sustained elevated ROS levels during the blastula and gastrula stages are essential for early vertebrate embryonic development, at least partly, through their roles in promoting growth factor signalling.

scholarly journals Nerve Growth Factor-induced Neuronal Differentiation Requires Generation of Rac1-regulated Reactive Oxygen Species

2000 ◽  
Vol 275 (18) ◽  
pp. 13175-13178 ◽  
Author(s):  
Kazumi Suzukawa ◽  
Koichi Miura ◽  
Junji Mitsushita ◽  
James Resau ◽  
Kunitaka Hirose ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Neuronal Differentiation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Nerve Growth

scholarly journals Initiation and Execution of Programmed Cell Death and Regulation of Reactive Oxygen Species in Plants

2021 ◽  
Vol 22 (23) ◽  
pp. 12942
Author(s):  
Chanjuan Ye ◽  
Shaoyan Zheng ◽  
Dagang Jiang ◽  
Jingqin Lu ◽  
Zongna Huang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Plant Stress ◽  
Reactive Oxygen ◽  
Signalling Pathways ◽  
Oxygen Species ◽  
Signalling Molecules ◽  
Plant Stress Tolerance ◽  
The Relationship

Programmed cell death (PCD) plays crucial roles in plant development and defence response. Reactive oxygen species (ROS) are produced during normal plant growth, and high ROS concentrations can change the antioxidant status of cells, leading to spontaneous cell death. In addition, ROS function as signalling molecules to improve plant stress tolerance, and they induce PCD under different conditions. This review describes the mechanisms underlying plant PCD, the key functions of mitochondria and chloroplasts in PCD, and the relationship between mitochondria and chloroplasts during PCD. Additionally, the review discusses the factors that regulate PCD. Most importantly, in this review, we summarise the sites of production of ROS and discuss the roles of ROS that not only trigger multiple signalling pathways leading to PCD but also participate in the execution of PCD, highlighting the importance of ROS in PCD.

scholarly journals Green tea polyphenols potentiate the action of nerve growth factor to induce neuritogenesis: Possible role of reactive oxygen species

2010 ◽  
Vol 88 (16) ◽  
pp. 3644-3655 ◽  
Author(s):  
Usha Gundimeda ◽  
Thomas H. McNeill ◽  
Jason E. Schiffman ◽  
David R. Hinton ◽  
Rayudu Gopalakrishna
Keyword(s):  
Reactive Oxygen Species ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Green Tea ◽  
Reactive Oxygen ◽  
Tea Polyphenols ◽  
Green Tea Polyphenols ◽  
Oxygen Species ◽  
Nerve Growth

scholarly journals Mitochondrial Reactive Oxygen Species Mediate GPCR–induced TACE/ADAM17-dependent Transforming Growth Factor-α Shedding

2009 ◽  
Vol 20 (24) ◽  
pp. 5236-5249 ◽  
Author(s):  
Timothy J. Myers ◽  
Leann H. Brennaman ◽  
Mary Stevenson ◽  
Shigeki Higashiyama ◽  
William E. Russell ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Ros Scavenging ◽  
Transforming Growth Factor Α ◽  
Egfr Activation ◽  
Mitochondrial Ros ◽  
Factor Α

Epidermal growth factor receptor (EGFR) activation by GPCRs regulates many important biological processes. ADAM metalloprotease activity has been implicated as a key step in transactivation, yet the regulatory mechanisms are not fully understood. Here, we investigate the regulation of transforming growth factor-α (TGF-α) shedding by reactive oxygen species (ROS) through the ATP-dependent activation of the P2Y family of GPCRs. We report that ATP stimulates TGF-α proteolysis with concomitant EGFR activation and that this process requires TACE/ADAM17 activity in both murine fibroblasts and CHO cells. ATP-induced TGF-α shedding required calcium and was independent of Src family kinases and PKC and MAPK signaling. Moreover, ATP-induced TGF-α shedding was completely inhibited by scavengers of ROS, whereas calcium-stimulated shedding was partially inhibited by ROS scavenging. Hydrogen peroxide restored TGF-α shedding after calcium chelation. Importantly, we also found that ATP-induced shedding was independent of the cytoplasmic NADPH oxidase complex. Instead, mitochondrial ROS production increased in response to ATP and mitochondrial oxidative complex activity was required to activate TACE-dependent shedding. These results reveal an essential role for mitochondrial ROS in regulating GPCR-induced growth factor shedding.

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