Neuroprotection by cord blood neural progenitors involves antioxidants, neurotrophic and angiogenic factors
| Autor: | Shimon Lecht, Hadar Arien-Zakay, Rinat Tabakman, Marian M. Bercu, Hanan Galski, Arnon Nagler, Philip Lazarovici, Ron Kohen |
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| Rok vydání: | 2008 |
| Předmět: |
medicine.medical_specialty
Free Radicals Basic fibroblast growth factor Neovascularization Physiologic Tropomyosin receptor kinase A Biology Neuroprotection PC12 Cells Antioxidants chemistry.chemical_compound Paracrine signalling Developmental Neuroscience Neurotrophic factors Internal medicine Cell Line Tumor medicine Animals Humans Nerve Growth Factors Angiogenic Proteins Autocrine signalling Cells Cultured Neurons Stem Cells Cell Differentiation Fetal Blood Coculture Techniques Cell biology Rats Stroke Oxidative Stress Nerve growth factor Endocrinology Phenotype Neurology chemistry Cytoprotection Hypoxia-Ischemia Brain biology.protein Oxidation-Reduction Neurotrophin |
| Zdroj: | Experimental neurology. 216(1) |
| ISSN: | 1090-2430 |
| Popis: | Human umbilical cord blood (HUCB) is a valuable source for cell therapy since it confers neuroprotection in stroke animal models. However, the responsible sub-populations remain to be established and the mechanisms involved are unknown. To explore HUCB neuroprotective properties in a PC12 cell-based ischemic neuronal model, we used an HUCB mononuclear-enriched population of collagen-adherent cells, which can be differentiated in vitro into a neuronal phenotype (HUCBNP). Upon co-culture with insulted-PC12 cells, HUCBNP conferred approximately 30% neuroprotection, as evaluated by decreased lactate dehydrogenase and caspase-3 activities. HUCBNP decreased by 95% the level of free radicals in the insulted-PC12 cells, in correlation with the appearance of antioxidants, as measured by changes in the oxidation-reduction potential of the medium using cyclic-voltammetry. An increased level of nerve growth factor (NGF), vascular endothelial growth factor and basic fibroblast growth factor in the co-culture medium was temporally correlated with a -medium neuroprotection effect, which was partially abolished by heat denaturation. HUCBNP-induced neuroprotection was correlated with changes in gene expression of these neurotrophic factors, while blocked by K252a, an antagonist of the TrkA/NGF receptor. These findings indicate that HUCBNP-induced neuroprotection involves antioxidant(s) and neurotrophic factors, which, by paracrine and/or autocrine interactions between the insulted-PC12 and the HUCBNP cells, conferred neuroprotection. |
| Databáze: | OpenAIRE |
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