Publication List English

Gap junction protein beta 4 plays an important role in cardiac function in humans, rodents, and zebrafish

A novel orexin antagonist from a natural plant was discovered using zebrafish behavioural analysis

C3orf70 Is Involved in Neural and Neurobehavioral Development

Generation of a Triple-Transgenic Zebrafish Line for Assessment of Developmental Neurotoxicity during Neuronal Differentiation

Aging-associated microstructural deterioration of vertebra in zebrafish

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


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


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.