Publication List English

2019/03/18
Zebrafish yolk sac microinjection of thalidomide for assessment of developmental toxicology

2019/02/18
Toxicological Evaluation of SiO2 Nanoparticles by Zebrafish Embryo Toxicity Test

2018/12/27
Increased susceptibility to oxidative stress-induced toxicological evaluation by genetically modified nrf2a-deficient zebrafish.

2018/01/18
EGF receptor kinase suppresses ciliogenesis through activation of USP8 deubiquitinase

2017/11/23
Chemokines protect vascular smooth muscle cells from cell death induced by cyclic mechanical stretch.

tHeme Oxygenase-1 Gene Induction as an Intrinsic Regulation against Delayed Cerebral Vasospasm in Rats.

                     
1999/01/01

Hidenori Suzuki, Kenji Kanamaru, Hiroshi Tsunoda, Hiroyasu Inada, Minoru Kuroki, Hong Sun, Shiro Waga and Toshio Tanaka
J. Clin. Invest. 104 59-66 1999

Abstract

Delayed cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) causes cerebral ischemia and infarction. To date, the pathogenesis and gene expression associated with vasospasm remain poorly understood. The present study used fluorescent differential display to identify differentially expressed genes in a rat model of SAH. By using quantitative RT-PCR, we found that heme oxygenase-1 (HO-1) mRNA was prominently induced in the basilar artery and modestly in brain tissue in a rat vasospasm model. A significant correlation was observed between the degree of vasospasm and HO-1 mRNA levels in the basilar arteries exhibiting vasospasm. Intracisternal injection of antisense HO-1 oligodeoxynucleotide (ODN) significantly delayed the clearance of oxyhemoglobin and deoxyhemoglobin from the subarachnoid space and aggravated angiographic vasospasm. Antisense HO-1 ODN inhibited HO-1 induction in the basilar arteries but not in the whole brain tissue. This phenomenon was not observed in the nontreated, sense HO-1 ODN-treated, or scrambled ODN-treated arteries. We report the protective effects of HO-1 gene induction in cerebral vasospasm after SAH, a finding that should provide a novel therapeutic approach for cerebral vasospasm.

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