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Nox4-mediated cell signaling regulates differentiation and survival of neural crest stem cells

Title
Nox4-mediated cell signaling regulates differentiation and survival of neural crest stem cells
Authors
Lee J.-E.Cho K.E.Lee K.E.Kim J.Bae Y.S.
Ewha Authors
배윤수김재상
SCOPUS Author ID
배윤수scopus; 김재상scopus
Issue Date
2014
Journal Title
Molecules and Cells
ISSN
1016-8478JCR Link
Citation
vol. 37, no. 12, pp. 907 - 911
Keywords
Bone morphogenetic proteinNeural crest stem cellNeuronal differentiationNox4Reactive oxygen species
Publisher
Korean Society for Molecular and Cellular Biology
Indexed
SCI; SCIE; SCOPUS; KCI WOS scopus
Abstract
The function of reactive oxygen species (ROS) as second messengers in cell differentiation has been demonstrated only for a limited number of cell types. Here, we used a wellestablished protocol for BMP2-induced neuronal differentiation of neural crest stem cells (NCSCs) to examine the function of BMP2-induced ROS during the process. We first show that BMP2 indeed induces ROS generation in NCSCs and that blocking ROS generation by pretreatment of cells with diphenyleneiodonium (DPI) as NADPH oxidase (Nox) inhibitor inhibits neuronal differentiation. Among the ROSgenerating Nox isozymes, only Nox4 was expressed at a detectable level in NCSCs. Nox4 appears to be critical for survival of NCSCs at least in vitro as down-regulation by RNA interference led to apoptotic response from NCSCs. Interestingly, development of neural crest-derived peripheral neural structures in Nox4-/- mouse appears to be grossly normal, although Nox4-/- embryos were born at a sub-Mendelian ratio and showed delayed over-all development. Specifically, cranial and dorsal root ganglia, derived from NCSCs, were clearly present in Nox4-/- embryo at embryonic days (E) 9.5 and 10.5. These results suggest that Nox4-mediated ROS generation likely plays important role in fate determination and differentiation of NCSCs, but other Nox isozymes play redundant function during embryogenesis. © The Korean Society for Molecular and Cellular Biology. All rights reserved.
DOI
10.14348/molcells.2014.0244
Appears in Collections:
자연과학대학 > 생명과학전공 > Journal papers
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