Protection of Hippocampal Neurons from Ischemia-Induced Delayed Neuronal Death by Hepatocyte Growth Factor: A Novel Neurotrophic Factor
Autor: | Tetsumori Yamashima, Takahito Miyazawa, Hidenori Ohmichi, Kunio Matsumoto, Hiroshi Katoh, Toshikazu Nakamura |
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Rok vydání: | 1998 |
Předmět: |
Male
Programmed cell death medicine.medical_specialty C-Met Neurite Apoptosis Hippocampal formation Hippocampus Neuroprotection Brain Ischemia 030218 nuclear medicine & medical imaging 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Neurotrophic factors Internal medicine medicine Animals Humans Cells Cultured Neurons Hepatocyte Growth Factor business.industry Cell Hypoxia Corpus Striatum Recombinant Proteins Neuroprotective Agents Endocrinology medicine.anatomical_structure nervous system Neurology chemistry Hepatocyte growth factor Neurology (clinical) Neuron Gerbillinae Cardiology and Cardiovascular Medicine business 030217 neurology & neurosurgery medicine.drug |
Zdroj: | Journal of Cerebral Blood Flow & Metabolism. 18:345-348 |
ISSN: | 1559-7016 0271-678X |
DOI: | 10.1097/00004647-199804000-00001 |
Popis: | Hepatocyte growth factor (HGF), a natural ligand for the c-met protooncogene product, exhibits mitogenic, motogenic, and morphogenic activities for regeneration of the liver, kidney, and lung. Recently, HGF was clearly shown to enhance neurite outgrowth in vitro. To determine whether HGF has a neuroprotective action against the death of neurons in vivo, we studied the effect of HGF on delayed neuronal death in the hippocampus after 5-minute transient forebrain ischemia in Mongolian gerbils. Continuous postischemic intrastriatal administration of human recombinant HGF (10 or 30 μg) for 7 days potently prevented the delayed death of hippocampal neurons under both anesthetized and awake conditions. Even when HGF infusion started 6 hours after ischemia (i.e., in a delayed manner), HGF exhibited a neuroprotective action. We conclude that HGF, a novel neurotrophic factor, has a profound neuroprotective effect against postischemic delayed neuronal death in the hippocampus, which may have implications for the development of new therapeutic strategies for ischemic neuronal damage in humans. |
Databáze: | OpenAIRE |
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