Linked Life Data

17459722

Source:http://linkedlifedata.com/resource/pubmed/id/17459722

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-6-5
pubmed:abstractText
Investigations regarding the regulation of adult neurogenesis, i.e., the generation of new neurons from progenitor cells, have revealed a high degree of complexity. Although the pleiotropic messenger molecule nitric oxide (NO) has been suggested to modulate adult neurogenesis, the evidence is inconclusive due to the presence of different NO synthase isoforms in the brain. We therefore investigated whether stem cell proliferation or survival is altered in mice lacking neuronal nitric oxide synthase (NOS-I) or both endothelial and neuronal NOS (NOS-I/-III double knockout). While proliferation of neural stem cells was only numerically, but not significantly increased in NOS-I knockdown animals, the survival of newly formed neurons was substantially higher in NOS-I-deficient mice. In contrast, NOS-I/-III double knockout had significantly decreased survival rates. QRT-PCR in NOS-I-deficient mice revealed neither NOS-III upregulation compensating for the loss of NOS-I, nor alterations in VEGF levels as found in NOS-III-deficient animals. As changes in BDNF expression or protein levels were observed in the cortex, cerebellum and striatum, but not the hippocampus, the increase in stem cell survival appears not to be due to a BDNF mediated mechanism. Finally, NOS-I containing neurons in the dentate gyrus are rare and not localized close to progenitor cells, rendering direct NO effects on these cells unlikely. In conclusion, we suggest that NO predominantly inhibits the survival of new-born cells, by an indirect mechanism not involving BDNF or VEGF. Together, these results emphasize the important role of the different NOS isoforms with respect to adult neurogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1044-7431
pubmed:author
pubmed:issnType
Print
pubmed:volume
35
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
261-71
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:17459722-Animals, pubmed-meshheading:17459722-Brain-Derived Neurotrophic Factor, pubmed-meshheading:17459722-Bromodeoxyuridine, pubmed-meshheading:17459722-Cell Proliferation, pubmed-meshheading:17459722-Cell Survival, pubmed-meshheading:17459722-Glial Fibrillary Acidic Protein, pubmed-meshheading:17459722-Hippocampus, pubmed-meshheading:17459722-Ki-67 Antigen, pubmed-meshheading:17459722-Mice, pubmed-meshheading:17459722-Mice, Knockout, pubmed-meshheading:17459722-Neurons, pubmed-meshheading:17459722-Nitric Oxide Synthase Type I, pubmed-meshheading:17459722-Nitric Oxide Synthase Type II, pubmed-meshheading:17459722-Nitric Oxide Synthase Type III, pubmed-meshheading:17459722-RNA, Messenger, pubmed-meshheading:17459722-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:17459722-Stem Cells, pubmed-meshheading:17459722-Vascular Endothelial Growth Factor A
pubmed:year
2007
pubmed:articleTitle
Neuronal nitric oxide synthase (NOS-I) knockout increases the survival rate of neural cells in the hippocampus independently of BDNF.
pubmed:affiliation
Molecular and Clinical Psychobiology, Department of Psychiatry and Psychotherapy Josef-Schneider-Str. 11, Julius-Maximilians-University Würzburg, Füchsleinstr. 15, D-97080 Würzburg, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't