Antisense preproendothelin-oligoDNA therapy for vasospasm in a canine model of subarachnoid hemorrhage

Ohkuma, Hiroki; Parney, Ian F.; Megyesi, Joseph F.; Ghahary, A.; Jm, Findlay

doi:10.3171/jns.1999.90.6.1105

Cited by 44 publications

(15 citation statements)

References 44 publications

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“…Even though Ohkuma et al 11 showed a mild reduction in vasospasm in a canine model using an antisense therapy, we observed a marked attenuation of vasospasm in the present study. Different observations between these 2 studies might be caused by differential targeting of mRNAs by antisense ODN.…”

Section: Antisense Therapy For Vasospasmsupporting

confidence: 29%

Inhibitory Effect With Antisense Mitogen-Activated Protein Kinase Oligodeoxynucleotide Against Cerebral Vasospasm in Rats

Satoh

Parent

Zhang

2002

Stroke

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Background and Purpose-Mitogen-activated protein kinase (MAPK) may be associated with the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH). This study aimed to clarify the role of MAPK expression and activation during cerebral vasospasm and to evaluate the therapeutic effect on cerebral vasospasm using an antisense MAPK oligodeoxynucleotide (ODN). Methods-Antisense MAPK, sense MAPK, or scrambled ODN was injected into the rats intracisternally. We used a single-hemorrhage experimental SAH model to assess vasospasm in the basilar arteries at 30 minutes, 1 day, and 2 days after SAH by cross-sectional area measurement and other histological parameters.

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Section: Antisense Therapy For Vasospasmsupporting

confidence: 29%

Inhibitory Effect With Antisense Mitogen-Activated Protein Kinase Oligodeoxynucleotide Against Cerebral Vasospasm in Rats

Satoh

Parent

Zhang

2002

Stroke

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“…10 -12 Third, antagonists of ET-1 attenuate vasospasm in experimental models of SAH. 2,[13][14][15] However, mechanisms of release, cellular origin, or even the compartment of release of ET-1 in SAH are still unknown. So far, production of ET-1 has been attributed to endothelial cells, 16 smooth muscle cells, 17 neurons, 18 or astrocytes.…”

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confidence: 99%

Endothelin-1 in Subarachnoid Hemorrhage

Faßbender

Hodapp

Rossol

et al. 2000

Stroke

142

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Background and Purpose-The most potent vasoconstrictor known, endothelin-1, is currently considered to mediate cerebral vasospasm in subarachnoid hemorrhage (SAH), which can cause delayed cerebral ischemia. In our study, we performed clinical and in vitro experiments to investigate the origin and the mechanisms of the secretion of endothelin-1 in SAH. Methods-Endothelin-1 and markers of inflammatory host response (interleukin [IL]-1␤, IL-6, and tumor necrosis factor-␣) were comparatively quantified in the cerebrospinal fluid (CSF) of SAH patients and control subjects, and concentrations were related to clinical characteristics. Furthermore, mononuclear leukocytes isolated from the CSF of SAH patients and control subjects were analyzed regarding their mRNA expression of endothelin-1 and inflammatory cytokines. Finally, complementary in vitro experiments were performed to investigate whether coincubation of blood and CSF can trigger leukocytic mRNA expression and release of these factors. Results-Activated mononuclear leukocytes in the CSF of SAH patients synthesize and release endothelin-1 in parallel with known acute-phase reactants (IL-1␤, IL-6, and tumor necrosis factor-␣). Complementary in vitro experiments not only further confirmed this leukocytic origin of endothelin-1 but also showed that aging and subsequent hemolysis of blood is sufficient to induce such endothelin-1 production. Conclusions-The demonstration that endothelin-1 is produced by activated CSF mononuclear leukocytes suggests that subarachnoid inflammation may represent a therapeutic target to prevent vasospasm and delayed cerebral ischemia after SAH. (Stroke. 2000;31:2971-2975.)

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“…We counted cells in each layer of the arterial wall at various times after SAH to determine if changes were due to an increase in number of cells and to establish whether genomic deoxyribonucleic acid (gDNA) could be used as a housekeeping standard. The results call into question literature reporting changes in gene expression after SAH (Hino et al, 1996b;Sayama et al, 1998;Ohkuma et al, 1999;Onda et al, 1999;Suzuki et al, 1999;Ono et al, 2000;Miyagi et al, 2000;Aihara et al, 2001) and suggest that there is significant cell proliferation within certain layers of the arterial wall after SAH in dogs.…”

Section: Introductionmentioning

confidence: 72%

“…The levels of mRNA for these genes has been assumed to be stable in some prior studies (Hino et al, 1996a;Sayama et al, 1998;Ohkuma et al, 1999;Onda et al, 1999;Suzuki et al, 1999;Ono et al, 2000;Miyagi et al, 2000;Aihara et al, 2001). If housekeeping gene mRNA increases, then genes reported to have increased expression might actually have been increased even more.…”

Section: Discussionmentioning

confidence: 99%

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Induction of housekeeping gene expression after subarachnoid hemorrhage in dogs

Aihara

Jahromi

Yassari

et al. 2008

Journal of Neuroscience Methods

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Changes in gene expression are commonly assessed relative to the expression of housekeeping genes, which are assumed to remain unchanged. We tested this assumption in cerebral arteries obtained from dogs 4 and 7 days after SAH had been created using the double hemorrhage model. Basilar arteries were removed and examined for expression of messenger ribonucleic acid (mRNA) levels using quantitative real-time polymerase chain reaction. Cross sections of basilar arteries were stained immunohistochemically for proliferating cell nuclear antigen (PCNA) and 4′,6-diamidino-2-phenylindole (DAPI). Positively-stained cells were counted and numbers obtained were normalized to the cross-sectional area. Results were compared to normal dog basilar arteries contracted pharmacologically in vitro. SAH resulted in significant vasospasm (P<0.001 for each, paired t-tests). There were significant increases in mRNA for β-actin (441%, P=0.01), glyceraldehyde-3-phosphate dehydrogenase (566%, P=0.007) and 18S ribosomal RNA (320%, P=0.025) 7 days after SAH. Total mRNA was increased 7 days after SAH relative to genomic DNA (157%, P=0.009). There were significant increases in the number of cells in the tunica media and adventitia of arteries after SAH and a significant decrease in the media after contraction in vitro. Cells in the tunica media and adventitia labeled with PCNA were significantly increased at both times after SAH. Transcripts for housekeeping genes are increased after SAH, making standardization to them potentially invalid. The increase is due to proliferation of cells in the adventitia and increased total mRNA in the media and adventitia.

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Antisense preproendothelin-oligoDNA therapy for vasospasm in a canine model of subarachnoid hemorrhage

Cited by 44 publications

References 44 publications

Inhibitory Effect With Antisense Mitogen-Activated Protein Kinase Oligodeoxynucleotide Against Cerebral Vasospasm in Rats

Inhibitory Effect With Antisense Mitogen-Activated Protein Kinase Oligodeoxynucleotide Against Cerebral Vasospasm in Rats

Endothelin-1 in Subarachnoid Hemorrhage

Induction of housekeeping gene expression after subarachnoid hemorrhage in dogs

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