The role of NADPH oxidases in neuronal development.

Aslihan Terzi, Daniel M Suter

Journal: Free radical biology & medicine 2021;154():33-47

PMID: 32370993

Full Text on Elsevier Science View on PubMed

Abstract

Reactive oxygen species (ROS) are critical for maintaining cellular homeostasis and function when produced in physiological ranges. Important sources of cellular ROS include NADPH oxidases (Nox), which are evolutionary conserved multi-subunit transmembrane proteins. Nox-mediated ROS regulate variety of biological processes including hormone synthesis, calcium signaling, cell migration, and immunity. ROS participate in intracellular signaling by introducing post-translational modifications to proteins and thereby altering their functions. The central nervous system (CNS) expresses different Nox isoforms during both development and adulthood. Here, we review the role of Nox-mediated ROS during CNS development. Specifically, we focus on how individual Nox isoforms contribute to signaling in neural stem cell maintenance and neuronal differentiation, as well as neurite outgrowth and guidance. We also discuss how ROS regulates the organization and dynamics of the actin cytoskeleton in the neuronal growth cone. Finally, we review recent evidence that Nox-derived ROS modulate axonal regeneration upon nervous system injury.

Address: Department of Biological Sciences, Purdue University, West Lafayette, IN, 47907, USA; Purdue Institute for Integrative Neuroscience, Purdue University, West Lafayette, IN, 47907, USA.; Department of Biological Sciences, Purdue University, West Lafayette, IN, 47907, USA; Purdue Institute for Integrative Neuroscience, Purdue University, West Lafayette, IN, 47907, USA; Bindley Bioscience Center, Purdue University, West Lafayette, IN, 47907, USA. Electronic address: [email protected].

DOI: 10.1016/j.freeradbiomed.2020.04.027

Link outs

Subscription / membership required

Full Text Sources:

MeSH Terms: Central Nervous System, NADPH Oxidases, Neurogenesis, Neurons, Reactive Oxygen Species