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

NADPH 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 R...

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Bibliographic Details
Published in:	Journal of neurochemistry Vol. 167; no. 4; pp. 505 - 519
Main Authors:	Alam, S M Sabbir, Watanabe, Yuichiro, Steeno, Brooke L, Dutta, Soumyajit, Szilagyi, Halie A, Wei, Alexander, Suter, Daniel M
Format:	Journal Article
Language:	English
Published:	England Blackwell Publishing Ltd 01-11-2023
Subjects:	Actin Actins Animals Aplysia Cones CYBB protein Growth cones Hydrogen peroxide Injury prevention Kinases NAD(P)H oxidase NADPH Oxidase 4 NADPH Oxidases - pharmacology Nervous system Neurites Neurodegeneration Neurogenesis Neurons Oxidase Physiological effects Protein-tyrosine kinase Reactive Oxygen Species Regeneration Tyrosine growth cone neurite regeneration NADPH oxidase hydrogen peroxide reactive oxygen species
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Summary:	NADPH 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 cultured Aplysia bag cell neurons. Using a novel hydrogen peroxide (H O )-sensing dye, 5'-(p-borophenyl)-2'-pyridylthiazole pinacol ester (BPPT), we found that H O levels are elevated in regenerating growth cones following injury. Redistribution of Nox2 and p40 in the growth cone central domain suggests Nox2 activation after injury. Inhibiting Nox with the pan-Nox inhibitor celastrol reduced neurite regeneration rate. Pharmacological inhibition of Nox is correlated with reduced activation of Src2 tyrosine kinase and F-actin content in the growth cone. Taken together, these findings suggest that Nox-derived ROS regulate neurite regeneration following injury through Src2-mediated regulation of actin organization in Aplysia growth cones.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Authors’ contributions S.A., Y.W., A.W., and D.S. designed the study. S.A., Y.W., B.S., S.D., and H.S. performed experiments. S.A., Y.W., B.S., S.D., A.W., and D.S. were involved with data analysis. S.A., Y.W., A.W. and D.S. wrote or edited the manuscript.
ISSN:	0022-3042 1471-4159 1471-4159
DOI:	10.1111/jnc.15977