Cited by 133Neurogenesis and neuroplasticity mechanismsRedox biology and oxidative stressCell death mechanisms and regulation

Newborn neurons acquire high levels of reactive oxygen species and increased mitochondrial proteins upon differentiation from progenitors

Tsatmali, Marina, Walcott, Elisabeth C., Crossin, Kathryn L.·2005·Brain Research

Abstract

A population of embryonic rat cortical cells cultured in the presence of FGF2 and having neuronal morphology expressed higher levels of reactive oxygen species (ROS) than did progenitor cells, astrocytes, and several cell lines of neuronal and non-neuronal origin. ROS were assessed using 5-(and-6)-chlormethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester (CM-H2DCF-DA), and high levels persisted in the presence of antioxidants or lowered levels of ambient oxygen. Greater than 95% of high ROS-producing cells, isolated by fluorescence-activated cell sorting, expressed the neuronal marker beta III tubulin. These cells did not incorporate BrdU or express nestin, unlike low ROS-producing cells, 99% of which exhibited both of these characteristics. Upon growth factor removal, low ROS-expressing cells differentiated into neurons and astrocytes and these neurons expressed high levels of ROS, indicating that ROS accumulation accompanies the differentiation of progenitors into neurons. ROS levels were decreased by added superoxide dismutase and catalase, suggesting that both superoxide and hydrogen peroxide contribute to the ROS signal. High ROS-expressing cells also contained higher levels of several mitochondrial respiratory chain components. Although ROS have been associated with conditions that lead to cell death, our results and recent studies on the role of ROS as regulators of signal pathways are consistent with the possibility that ROS play a role in the development of the neuronal phenotype. Moreover, the differential production of ROS provides a useful method to isolate from mixed populations cells that are highly enriched for either progenitor cells or neurons.

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Crossref · 10.1016/j.brainres.2005.01.087

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Authors
Tsatmali, M., Walcott, E. C., & Crossin, K. L.
Affiliations
  • Scripps Research Institute (US)
  • Neurosciences Institute (US)
Corresponding author
Crossin, Kathryn L.
Venue
Brain Research
Publisher
Elsevier BV
Published
2005-04
Volume
1040
Issue
1-2
Pages
137-150
ISSN
0006-8993 (ISSN-L)
OpenAlex
W2002030791
Cited by
133
References
98
Citations by year
2025: 4 · 2023: 2 · 2022: 5 · 2021: 3 · 2020: 9 · 2019: 4 · 2018: 6 · 2017: 9 · 2016: 10 · 2015: 14 · 2014: 5 · 2013: 12 · 2012: 15
FWCI
1.22
Type
journal article
Language
en
Open access
closed
Locations
  • Brain Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
reactive oxygen species, neuronal differentiation, neural progenitor cells, newborn neurons, cortical development, FGF2, TUBB3, superoxide, hydrogen peroxide, mitochondrial respiratory chain, superoxide dismutase, catalase, astrocytes, cell isolation, oxidative stress signaling
MeSH terms
Animals, Animals, Newborn, Cell Differentiation, Cells, Cultured, Female, Neurons, Pregnancy, Stem Cells, Rats, Wistar, Reactive Oxygen Species, Mitochondrial Proteins, Rats

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