Mice expressing a bovine basic fibroblast growth factor transgene in the brain show increased resistance to hypoxemic-ischemic cerebral damage.

MacMillan, V.; Judge, Daniel P.; Wiseman, Amy L.; Settles, Deann C.; Swain, Judith L.; Davis, James N.

doi:10.1161/01.str.24.11.1735

Cited by 55 publications

(14 citation statements)

References 23 publications

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“…13,15,[27][28][29] However, mouse SAH models have never been reported because of the technical difficulties in making a reliable model, although a number of SAH model in rats are available for research on SAH. 30 -34 Recently, new rat SAH models without craniectomy have been developed on the basis of an endovascular perforation of the cerebral artery.…”

Section: Discussionmentioning

confidence: 99%

Amelioration of Vasospasm After Subarachnoid Hemorrhage in Transgenic Mice Overexpressing CuZn–Superoxide Dismutase

Kamii

Kato

Kinouchi

et al. 1999

Stroke

129

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Background and Purpose-To clarify the effect of superoxide dismutase (SOD) on vasospasm after subarachnoid hemorrhage (SAH), we investigated sequential changes in arterial diameter after SAH in transgenic mice overexpressing CuZn-SOD (SOD-1). Methods-SOD-transgenic mice and nontransgenic littermates (35 to 40 g) were subjected to SAH produced by endovascular perforation of left anterior cerebral artery. At 4 hours and 1, 3, 7, and 14 days after SAH, the mice were perfused with 10% formalin and consequently with a mixture of carbon black and 10% gelatin to cast all vessels. Vasospasm was evaluated by measuring the diameter of the left middle cerebral artery (MCA) with a microscope. Results-In nontransgenic mice, the diameter of the MCA on day 3 after SAH (110.5Ϯ20.5 m [meanϮSD]; nϭ16) was significantly reduced compared with that without SAH (138.5Ϯ14.5 m; nϭ12) (PϽ0.01). Moreover, on day 3 after SAH, the diameter of the MCA in SOD-transgenic mice (127.9Ϯ20.2 m; nϭ20) was significantly larger than that in nontransgenic mice (110.5Ϯ20.5 m; nϭ16) (PϽ0.05). Conclusions-These results suggest that SOD is effective on the amelioration of vasospasm after SAH and that oxygen free radicals, particularly superoxide, play an important role in the pathogenesis of vasospasm after SAH. (Stroke. 1999;30:867-872.)Key Words: free radicals Ⅲ mice, transgenic Ⅲ subarachnoid hemorrhage Ⅲ superoxide dismutase Ⅲ vasospasm E rythrocytes are essential for causing vasospasm, and oxyhemoglobin released from erythrocytes in the subarachnoid clot is believed to be a most potent trigger of vasospasm. 1,2 However, the pathophysiology of cerebral vasospasm after subarachnoid hemorrhage (SAH) still remains unclear. Recently, 2 major derangements in the cerebral artery have been indicated as a cause for cerebral vasospasm after SAH. One is augmentation of contraction, which is protein kinase C (PKC) dependent, and the other is suppression of dilation, which is mediated by endothelium-derived relaxing factor/nitric oxide (NO). 3 Oxygen free radicals are involved in both systems; active oxygens can activate the PKC system and lead to lipid peroxidation through activation of phospholipase A 2 , 4 and superoxide (O 2 Ϫ ) is known to inactivate NO, 5 resulting in the occurrence of vasospasm after SAH. Therefore, superoxide dismutase (SOD), an enzyme converting O 2 Ϫ to hydrogen peroxide (H 2 O 2 ), could prevent contraction of the cerebral artery after SAH. Experiments in vivo, however, have not always proven the efficacy of SOD in preventing vasospasm after SAH. Kamiyama et al 6 See Editorial Comment, page 872initially showed that SOD is effective against vasospasm induced by oxyhemoglobin in cats. In addition, intracisternal injection of SOD reduced endothelial injury and prevented the occurrence of vasospasm in a rabbit SAH model. 7 However, intrathecal administration of both SOD and catalase failed to protect against oxyhemoglobin-induced vasospasm in monkeys. 8 The discrepancy in the effect of SOD on vasospasm after SAH may result from difference...

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Section: Discussionmentioning

confidence: 99%

Amelioration of Vasospasm After Subarachnoid Hemorrhage in Transgenic Mice Overexpressing CuZn–Superoxide Dismutase

Kamii

Kato

Kinouchi

et al. 1999

Stroke

129

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“…FGF-2 may play an important role in regeneration after injury of the CNS (251) as FGF-2 attenuates ischemic damage in mice (252). Transgenic mice that overexpress 18-kDa FGF-2 show a significantly higher number of surviving neurons after ischemia than do nontransgenic mice.…”

Section: February 1997mentioning

confidence: 99%

Biological Roles of Fibroblast Growth Factor-2*

et al. 1997

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“…Transgenic mice expressing high levels of specific gene products have increased resistance to cerebral ischemia (4,5) or have enhanced myocardial function (6). In fact, heat shock-induced changes in gene expression have been associated with cellular protection and improved function for more than a decade (7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

Transgenic mice expressing the human heat shock protein 70 have improved post-ischemic myocardial recovery.

et al. 1995

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Mice expressing a bovine basic fibroblast growth factor transgene in the brain show increased resistance to hypoxemic-ischemic cerebral damage.

Cited by 55 publications

References 23 publications

Amelioration of Vasospasm After Subarachnoid Hemorrhage in Transgenic Mice Overexpressing CuZn–Superoxide Dismutase

Amelioration of Vasospasm After Subarachnoid Hemorrhage in Transgenic Mice Overexpressing CuZn–Superoxide Dismutase

Biological Roles of Fibroblast Growth Factor-2*

Transgenic mice expressing the human heat shock protein 70 have improved post-ischemic myocardial recovery.

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