Neuronal NADPH oxidase is required for neurite regeneration of Aplysia bag cell neurons

In this study, we investigated the role of NADPH oxidase (Nox)-derived reactive oxygen species (ROS) in neuronal regeneration following mechanical injury. We found that in vitro injury triggers higher H2O2 levels and Nox2 and Src2 activation state in regenerating growth cones of culturedAplysia bag cell neurons. Inhibition of Nox by celastrol decreased neurite regeneration rate as well as Src2 activation and F-actin content. Our data indicate that ROS derived from neuronal Nox is required for the regeneration ofAplysia bag cell neurites. AbstractNADPH oxidase (Nox), a major source of reactive oxygen species (ROS), is involved in neurodegeneration after injury and disease. Nox is expressed in both neuronal and non-neuronal cells and contributes to an elevated ROS level after injury. Contrary to the well-known damaging effect of Nox-derived ROS in neurodegeneration, recently a physiological role of Nox in nervous system development including neurogenesis, neuronal polarity, and axonal growth has been revealed. Here, we tested a role for neuronal Nox in neurite regeneration following mechanical transection in culturedAplysia bag cell neurons. Using a novel hydrogen peroxide (H2O2)-sensing dye, 5 ′-(p-borophenyl)-2 ′-pyridylthiazole pinacol ester (BPPT), we found that H2O2 levels are elevated in regenerating growth cones following injury. Redistribution of Nox2 and p40phox in the growth cone central domain suggests Nox2 activation after injury. Inhibiting Nox with the pan-Nox...
Source: Journal of Neurochemistry - Category: Neuroscience Authors: Tags: ORIGINAL ARTICLE Source Type: research