Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
45
pubmed:dateCreated
2004-11-11
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
10
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
10201-10
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:15537892-Animals, pubmed-meshheading:15537892-Cell Cycle, pubmed-meshheading:15537892-Cell Division, pubmed-meshheading:15537892-Cerebral Cortex, pubmed-meshheading:15537892-Female, pubmed-meshheading:15537892-G1 Phase, pubmed-meshheading:15537892-Gestational Age, pubmed-meshheading:15537892-Humans, pubmed-meshheading:15537892-Insulin-Like Growth Factor I, pubmed-meshheading:15537892-Intermediate Filament Proteins, pubmed-meshheading:15537892-Mice, pubmed-meshheading:15537892-Mice, Inbred C3H, pubmed-meshheading:15537892-Mice, Inbred C57BL, pubmed-meshheading:15537892-Mice, Transgenic, pubmed-meshheading:15537892-Nerve Tissue Proteins, pubmed-meshheading:15537892-Pregnancy, pubmed-meshheading:15537892-Rats, pubmed-meshheading:15537892-Recombinant Fusion Proteins, pubmed-meshheading:15537892-Telencephalon, pubmed-meshheading:15537892-Time Factors, pubmed-meshheading:15537892-Transgenes
pubmed:year
2004
pubmed:articleTitle
Insulin-like growth factor-I accelerates the cell cycle by decreasing G1 phase length and increases cell cycle reentry in the embryonic cerebral cortex.
pubmed:affiliation
Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V5Z 4H4.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural