Relationship between reactive oxygen species and heme metabolism during the differentiation of Neuro2a cells

Although neuronal cells are highly vulnerable to oxidative stress, recent studies suggest that production of reactive oxygen species (ROS) increases during and is essential for neuronal differentiation. In addition, we have previously found that heme biosynthesis is up-regulated during retinoic acid...

Full description

Saved in:
Bibliographic Details
Published in:Biochemical and biophysical research communications 2007-06, Vol.358 (1), p.130-135
Main Authors: Shinjyo, Noriko, Kita, Kiyoshi
Format: Article
Language:English
Subjects:
Animals
Antioxidants - metabolism
Catalase
Catalase - metabolism
Cell Differentiation
Cells, Cultured
Differentiation
Heme
Heme - metabolism
Heme oxygenase
Heme Oxygenase (Decyclizing) - metabolism
Heme Oxygenase-1 - metabolism
Mice
Neuron
Neurons - cytology
Neurons - metabolism
Peroxisomes - metabolism
Reactive Oxygen Species - metabolism
ROS
Up-Regulation
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Although neuronal cells are highly vulnerable to oxidative stress, recent studies suggest that production of reactive oxygen species (ROS) increases during and is essential for neuronal differentiation. In addition, we have previously found that heme biosynthesis is up-regulated during retinoic acid-induced differentiation of Neuro2a cells. In the current study, we showed that this up-regulation of heme biosynthesis during differentiation is ROS-dependent. Furthermore, we found that ROS-dependent induction of heme oxygenase, which degrades heme and acts as an anti-oxidant, and catalase, another anti-oxidant enzyme that contains heme as a prosthetic group, occurs during differentiation. These results suggest that heme biosynthesis following the degradation of heme protects Neuro2a cells from oxidative stress caused by ROS during differentiation.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2007.04.071