Dissecting the role of redox signaling in neuronal development.
Daniel A BórquezPamela J UrrutiaCarlos WilsonBrigitte van ZundertMarco Tulio NúñezChristian Gonzalez-BillaultPublished in: Journal of neurochemistry (2016)
The generation of abnormally high levels of reactive oxygen species (ROS) is linked to cellular dysfunction, including neuronal toxicity and neurodegeneration. However, physiological ROS production modulates redox-sensitive roles of several molecules such as transcription factors, signaling proteins, and cytoskeletal components. Changes in the functions of redox-sensitive proteins may be important for defining key aspects of stem cell proliferation and differentiation, neuronal maturation, and neuronal plasticity. In neurons, most of the studies have been focused on the pathological implications of such modifications and only very recently their essential roles in neuronal development and plasticity has been recognized. In this review, we discuss the participation of NADPH oxidases (NOXs) and a family of protein-methionine sulfoxide oxidases, named molecule interacting with CasLs, as regulated enzymatic sources of ROS production in neurons, and describes the contribution of ROS signaling to neurogenesis and differentiation, neurite outgrowth, and neuronal plasticity. We review the role of reactive oxygen species (ROS) in neurogenesis, axon growth, and guidance and NMDA-receptor-mediated plasticity, LTP, and memory. ROS participation is presented in the context of NADPH oxidase and MICAL functions and their importance for brain functions.
Keyphrases
- reactive oxygen species
- cerebral ischemia
- cell death
- dna damage
- cell proliferation
- transcription factor
- subarachnoid hemorrhage
- oxidative stress
- spinal cord
- working memory
- spinal cord injury
- hydrogen peroxide
- amino acid
- functional connectivity
- drinking water
- neural stem cells
- optical coherence tomography
- electron transfer