고재영 (울산의대) | 상위피인용논문 > 한빛사

상위피인용논문

조회594

울산의대

Science, 23 Apr 1999 • Vol 284, Issue 5414 • pp. 647-650 | DOI: 10.1126/science.284.5414.647 Nonproteolytic Neuroprotection by Human Recombinant Tissue Plasminogen Activator

Yang-Hee Kim,^1,2 June-Hee Park,¹ Seung Hwan Hong,² Jae-Young Koh^1,*

¹National Creative Research Initiative Center for the Study of Central Nervous System Zinc and Department of Neurology, University of Ulsan College of Medicine, 388-1 Poongnap-Dong Songpa-Gu, Seoul 138-736, Korea. ²Department of Molecular Biology and Institute for Molecular Biology and Genetics, Seoul National University, Seoul, Korea.

^*To whom correspondence should be addressed.

Abstract

Human recombinant tissue plasminogen activator (tPA) may benefit ischemic stroke patients by dissolving clots. However, independent of thrombolysis, tPA may also have deleterious effects on neurons by promoting excitotoxicity. Zinc neurotoxicity has been shown to be an additional key mechanism in brain injuries. Hence, if tPA affects zinc neurotoxicity, this may provide additional insights into its effect on neuronal death. Independent of its proteolytic action, tPA markedly attenuated zinc-induced cell death in cortical culture, and, when injected into cerebrospinal fluid, also reduced kainate seizure–induced hippocampal neuronal death in adult rats.

논문정보