Antisense oligonucleotide eliminates in vivo expression of c-fos in mammalian brain

Chiasson, Bernard J.; Hooper, Michele L.; Murphy, Paul R.; Robertson, Harold A.

doi:10.1016/0922-4106(92)90167-t

Cited by 158 publications

(60 citation statements)

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“…Previous studies have demonstrated that the antisense c-fos oligonucleotide inhibits Fos production in the brain induced by various stimuli when it was injected 4 to 12 h before the test stimulus (Chiasson et al, 1992;Heilig et al, 1993;Hooper et al, 1994;Hunter et al, 1995;Morrow et al, 1999), whereas the same antisense c-fos oligonucleotide failed to suppress amphetamine-induced Fos expression in the striatum when it was injected 22 h before amphetamine injection (Chiasson et al, 1992). In the present study, the maze training was started 12 h after the antisense treatment, and it took ‫2ف‬ h. Therefore, it is unclear whether Fos production was inhibited by the antisense treatment during the entire time of training.…”

Section: Discussionmentioning

confidence: 99%

A Role of Fos Expression in the CA3 Region of the Hippocampus in Spatial Memory Formation in Rats

Yamada

Nabeshima

2002

Neuropsychopharmacology

115

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Section: Discussionmentioning

confidence: 99%

A Role of Fos Expression in the CA3 Region of the Hippocampus in Spatial Memory Formation in Rats

Yamada

Nabeshima

2002

Neuropsychopharmacology

115

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“…Inhibition of c-fos translation in the presence of anti-sense c-fos oligodeoxynudeotide. (A) A full length c-fos mRNA (0.6 μg) was translated using rabbit reticulocyte lysate and { 35 S} methionine with RNasin in the absence (lane 1 or in the presence of antisense oligodeoxynudeotide (10 pmol of anti-rncfosr 115 in lanes 2 and 3 or anti-rncfosr 143 in lanes 4 and 5). The peptide was immunoprecipitated by Ab-2 and protein A-agarose and then resolved in sodium dodecyl sulfate-polyacrylamide gel electrophoresis (7.5%).…”

Section: Discussionmentioning

confidence: 99%

“…Subsequently, standard desalting was used routinely in this study. 35 S at > 1,000 Ci/mmol and 5 mCi/ml)] was added to each reaction mixture and incubated for 5 minutes at room temperature, followed by an addition of the lysate (14 μl). The reaction was carried out at 30°C for 60 minutes.…”

Section: Methodsmentioning

confidence: 99%

“…The oligonucleotides employed in the antisense strategies are usually singlestranded DNA, 15 to 30 nucleotides in length. Anti-sense oligodeoxynucleotides have been used to suppress the expression of c-fos gene in cell culture systems [28][29][30][31][32][33][34] and in an animal model [35]. The antisense oligodeoxynucleotides are designed to block selected events such as transcription, splicing, or translation of the target mRNA.…”

Section: Nih Public Accessmentioning

confidence: 99%

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Suppression of ischemia‐induced fos expression and AP‐1 activity by an antisense oligodeoxynucleotide to c‐fos mRNA

Liu

Salminen

et al. 1994

Annals of Neurology

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Activation of c-fos, an immediate early gene, and the subsequent expression of the Fos protein have been noted following focal cerebral ischemia. Fos and Jun form a heterodimer as activator protein 1 (AP-1), which transregulates the expression of several genes. To study the postischemic events related to c-fos expression, we suppressed the expression of c-fos by intraventricular infusion of an antisense Oligodeoxynucleotide (anti-rncfosr 115 ) of c-fos mRNA. The effectiveness of antirncfosr 115 was confirmed first by its capability to block in vitro c-fos mRNA translation. In vivo, after intraventricular infusion of 32 P-labeled anti-rncfosr 115 , the oligodeoxynucleotide was internalized within 6 hours and detectable also in the nucleic acids fraction up to 41 hours. Treatment of the recovered nucleic acids with RNase H separated the labeled Oligodeoxynucleotide from the nucleic acid fraction, indicating an association of the antisense Oligodeoxynucleotide and cellular RNA after uptake. When focal cerebral ischemia was induced 16 hours after the infusion of antirncfosr 115 , the postischemic increase in Fos expression and AP-1 binding activity were suppressed. Specificity of the effect of anti-rncfosr 115 was suggested by its failure to suppress the DNA binding activity of nuclear cyclic AMP response elements. These results support the hypothesis that increased AP-1 binding activity following focal cerebral ischemia is dependent on Fos expression and can be inhibited in vivo by antisense c-fos oligodeoxynucleotides.The molecular events of brain adaptation to injury that may underlie functional recovery after stroke remain largely undefined. Recent observations of altered gene expression in ischemic brain using animal stroke models have opened new avenues for exploration of the biochemical cascades after stroke [1][2][3][4][5][6][7][8][9][10][11]. These postischemic events include an increase in extracellular excitatory amino acid neurotransmitters such as glutamate. Glutamate receptor-mediated activation of phospholipases and protein kinases results in the alteration of nuclear regulatory processes, including the expression of immediate early genes such as c-fos, junB, and c-jun [5,12]. The Fos, Jun, and JunB proteins have been shown to form activator protein 1 (AP-1) through a conserved dimerization domain, i.e., the leucine zipper [13]. Transcription regulator AP-1 protein binds a specific DNA motif and is believed to transactivate the expression of a number of late effector genes [14][15][16][17][18][19]. In the ischemic brain, we have previously demonstrated an increase in AP-1 binding activity [9]. A number of genes that bear neurotrophic properties may be regulated by transcription regulator AP-1. These genes, such as heat shock protein [1,4,[19][20][21][22], amyloid [23], neurotrophins [7], and protein tyrosine kinase receptor trkB [24], have been shown to be induced following cerebral ischemia. The causal relationship between the Fos/Jun-AP-1 cascade and the subsequent expression of the late e...

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“…A common strategy in ANTISENSE oligonucleotide design is to target the region around the AUG initiation codon (van der Krol et al 1988). Many of the successful experiments with ANTISENSE oligonucleotides published to date have used this approach (Fagarasan et al 1990;Listerud et al 1991;Chiasson et al 1992;Gyurko et al 1993;Heilig et al 1993;Lucas et al 1993;McCarthy et al 1993b;Wahlestedt et al 1993a,b;Zhang & Creese 1993;Suzuki et al 1994). …”

Section: Choice Of Antisensementioning

confidence: 99%

Untitled

1994

Clin Exp Pharma Physio

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SUMMARY1. Recent studies have shown that gene expression can be selectively attenuated by administration of short sequences of nucleotides (oligonucleotides) that are complementary to a portion of messenger RNA coding for a particular gene product.2. This technique is known as ANTISENSE, because the oligonucleotides are complementary to the mRNA which has the same sequence as the SENSE strand of DNA.3. In the present review we focus, after a brief discussion of gene expression and mechanisms of action of ANTISENSE, on the methodological aspects of ANTISENSE experiments in neuroscience. In particular, we address the advantages, disadvantages and controls for the ANTISENSE technique, as well as the choice, design, mode of delivery, dose and storage of ANTISENSE oligonucleotides.

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Antisense oligonucleotide eliminates in vivo expression of c-fos in mammalian brain

Cited by 158 publications

References 6 publications

A Role of Fos Expression in the CA3 Region of the Hippocampus in Spatial Memory Formation in Rats

A Role of Fos Expression in the CA3 Region of the Hippocampus in Spatial Memory Formation in Rats

Suppression of ischemia‐induced fos expression and AP‐1 activity by an antisense oligodeoxynucleotide to c‐fos mRNA

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