Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
|
pubmed:dateCreated |
1999-2-25
|
pubmed:abstractText |
We examined the uptake and distribution of an antisense phosphorothioated oligodeoxynucleotide (s-ODN) to c-fos, rncfosr115, infused into the left cerebral ventricle of male Long-Evans rats and the effect of this s-ODN on subsequent Fos, NGF, neurotrophin-3 (NT-3), and actin expression. To establish the uptake and turnover of s-ODN in the brain, we studied the copurification of the immunoreactivity of biotin with biotinylated s-ODN that was recovered from different regions of the brain. A time-dependent diffusion and the localization of s-ODN were further demonstrated by labeling the 3'-OH terminus of s-ODN in situ with digoxigenin-dUTP using terminal transferase and detection using anti-digoxigenin IgG-FITC. Cellular uptake of the s-ODN was evident in both the hippocampal and cortical regions, consistent with a gradient originating at the ventricular surface. Degradation of the s-ODN was observed beginning 48 hr after delivery. The effectiveness of c-fos antisense s-ODN was demonstrated by its suppression of postischemic Fos expression, which was accompanied by an inhibition of ischemia-induced NGF mRNA expression in the dentate gyrus. Infusion of saline, the sense s-ODN, or a mismatch antisense s-ODN did not suppress Fos expression. That this effect of c-fos antisense s-ODN was specific to NGF was demonstrated by its lack of effect on the postischemic expression of the NT-3 and beta-actin genes. Our results demonstrate that c-fos antisense s-ODN blocks selected downstream events and support the contention that postischemic Fos regulates the subsequent expression of the NGF gene and that Fos expression may have a functional component in neuroregeneration after focal cerebral ischemia-reperfusion.
|
pubmed:grant |
http://linkedlifedata.com/resource/pubmed/grant/NS25545,
http://linkedlifedata.com/resource/pubmed/grant/NS28995,
http://linkedlifedata.com/resource/pubmed/grant/NS34810,
http://linkedlifedata.com/resource/pubmed/grant/R01 NS034810-04,
http://linkedlifedata.com/resource/pubmed/grant/R01 NS034810-04S1
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Actins,
http://linkedlifedata.com/resource/pubmed/chemical/Biotin,
http://linkedlifedata.com/resource/pubmed/chemical/Nerve Growth Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Neurotrophin 3,
http://linkedlifedata.com/resource/pubmed/chemical/Oligonucleotides, Antisense
|
pubmed:status |
MEDLINE
|
pubmed:month |
Feb
|
pubmed:issn |
0270-6474
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
15
|
pubmed:volume |
19
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1335-44
|
pubmed:dateRevised |
2011-3-16
|
pubmed:meshHeading |
pubmed-meshheading:9952411-Actins,
pubmed-meshheading:9952411-Animals,
pubmed-meshheading:9952411-Biotin,
pubmed-meshheading:9952411-Brain Ischemia,
pubmed-meshheading:9952411-Depression, Chemical,
pubmed-meshheading:9952411-Gene Expression,
pubmed-meshheading:9952411-Genes, fos,
pubmed-meshheading:9952411-Hippocampus,
pubmed-meshheading:9952411-Immunohistochemistry,
pubmed-meshheading:9952411-In Situ Hybridization,
pubmed-meshheading:9952411-Male,
pubmed-meshheading:9952411-Nerve Growth Factors,
pubmed-meshheading:9952411-Neurotrophin 3,
pubmed-meshheading:9952411-Oligonucleotides, Antisense,
pubmed-meshheading:9952411-Rats,
pubmed-meshheading:9952411-Reverse Transcriptase Polymerase Chain Reaction
|
pubmed:year |
1999
|
pubmed:articleTitle |
Suppression of postischemic hippocampal nerve growth factor expression by a c-fos antisense oligodeoxynucleotide.
|
pubmed:affiliation |
Department of Neurosurgery, Baylor College of Medicine, Houston, Texas 77030, USA.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
|