Document Detail


Insulin-like growth factor-I accelerates the cell cycle by decreasing G1 phase length and increases cell cycle reentry in the embryonic cerebral cortex.
MedLine Citation:
PMID:  15537892     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Neurogenesis in the developing cerebral cortex of mice occurs in the dorsal telencephalon between embryonic day 11 (E11) and E17, during which time the majority of cortical projection neurons and some glia are produced from proliferating neuroepithelial cells in the ventricular zone. The number of cells produced by this process is governed by several factors, including cell cycle kinetics and the proportion of daughter cells exiting the cell cycle after a given round of cell division. The in vivo effects of IGF-I on cell cycle kinetics were investigated in nestin/IGF-I transgenic (Tg) embryos, in which IGF-I is overexpressed in the cerebral cortex and dorsal telencephalon. These Tg mice have been shown to exhibit increased cell number in the cortical plate by E16 and increased numbers of neurons and glia in the cerebral cortex during postnatal development. Cumulative S phase labeling with 5-bromo-2'-deoxyuridine revealed a decrease in total cell cycle length (TC) in Tg embryos on E14. This decrease in TC was found to result entirely from a reduction in the length of the G1 phase of the cell cycle from 10.66 to 8.81 hr, with no significant changes in the lengths of the S, G2, and M phases. Additionally, the proportion of daughter cells reentering the cell cycle was significantly increased by 15% in Tg embryos on E14-E15 compared with littermate controls. These data demonstrate that IGF-I regulates progenitor cell division in the ventricular zone by reducing G1 phase length and decreasing TC but increases cell cycle reentry.
Authors:
Rebecca D Hodge; A Joseph D'Ercole; John R O'Kusky
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of neuroscience : the official journal of the Society for Neuroscience     Volume:  24     ISSN:  1529-2401     ISO Abbreviation:  J. Neurosci.     Publication Date:  2004 Nov 
Date Detail:
Created Date:  2004-11-11     Completed Date:  2005-06-10     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8102140     Medline TA:  J Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  10201-10     Citation Subset:  IM    
Affiliation:
Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V5Z 4H4.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Cell Cycle / physiology
Cell Division / physiology
Cerebral Cortex / cytology*,  embryology,  metabolism
Female
G1 Phase / physiology*
Gestational Age
Humans
Insulin-Like Growth Factor I / genetics,  physiology*
Intermediate Filament Proteins / genetics
Mice
Mice, Inbred C3H
Mice, Inbred C57BL
Mice, Transgenic
Nerve Tissue Proteins / genetics
Pregnancy
Rats
Recombinant Fusion Proteins / physiology
Telencephalon / cytology*,  embryology,  metabolism
Time Factors
Transgenes
Grant Support
ID/Acronym/Agency:
HD08299/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Intermediate Filament Proteins; 0/Nerve Tissue Proteins; 0/Recombinant Fusion Proteins; 0/nestin; 67763-96-6/Insulin-Like Growth Factor I

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Synaptic targeting by Alzheimer's-related amyloid beta oligomers.
Next Document:  Role of mitogen-activated protein kinase activation in injured and intact primary afferent neurons f...