Folate stimulates ERK1/2 phosphorylation and cell proliferation in fetal neural stem cells

Cellular events for neural progenitor cells, such as proliferation and differentiation, are regulated by multiple intrinsic and extrinsic cell signals. Folate plays central roles in central nervous system development, so folate, as an extrinsic signal, may affect neural stem cell (NSC) proliferation...

Full description

Saved in:
Bibliographic Details
Published inNutritional neuroscience Vol. 12; no. 5; pp. 226 - 232
Main Authors Zhang, Xu-Mei, Huang, Guo-Wei, Tian, Zhi-Hong, Ren, Da-Lin, Wilson, John X.
Format Journal Article
LanguageEnglish
Published England Taylor & Francis 01.10.2009
Subjects
Analysis of Variance
Animals
APOPTOSIS
Brain - cytology
Brain - embryology
Brain - metabolism
Cell Proliferation
Cells, Cultured
EXTRACELLULAR SIGNAL-REGULATED KINASE
Fetal Stem Cells - cytology
Fetal Stem Cells - metabolism
FOLATE
Folic Acid - administration & dosage
Intermediate Filament Proteins - metabolism
Mitogen-Activated Protein Kinase 1 - metabolism
Mitogen-Activated Protein Kinase 3 - metabolism
Nerve Tissue Proteins - metabolism
Nestin
NEURAL STEM CELLS
Neurogenesis
Neuroglia - cytology
Neuroglia - metabolism
Neurons - cytology
Neurons - metabolism
Phosphorylation
PROLIFERATION
Rats
Rats, Sprague-Dawley
Online AccessGet full text

Cover

More Information
Summary:Cellular events for neural progenitor cells, such as proliferation and differentiation, are regulated by multiple intrinsic and extrinsic cell signals. Folate plays central roles in central nervous system development, so folate, as an extrinsic signal, may affect neural stem cell (NSC) proliferation and differentiation. In this study, we have investigated the effect of folate on extracellular signal-regulated kinase (ERK1/2) phosphorylation, cell proliferation and apoptosis in fetal NSCs. The results showed that treatment of neurospheres with folate increased ERK1/2 phosphorylation and cell proliferation in a concentration-dependent manner. Folate also decreased the percentage of apoptotic cells. All of these effects of folate were prevented by a selective inhibitor (U0126) of mitogen-activated/ERK kinase 1/2. In conclusion, fetal NSCs respond to folate with ERKl/2 phosphorylation, cell proliferation and decreased apoptosis. This mechanism may mediate the regulation by folate of neurogenesis in the central nervous system.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1028-415X
1476-8305
DOI:10.1179/147683009X423418