S100b protects IMR-32 cells against Ab(1-42) induced neurotoxicity via modulation of apoptotic genes expression
S100b protects IMR-32 cells against Ab(1-42) induced neurotoxicity via modulation of apoptotic genes expression作者机构：1CNR-ICRM Institute of Chimica del Riconoscimento Molecolare Department for Innovation in Biological Agro-food and Forest Systems (DIBAF) Tuscia University Viterbo Italy Institute of Biochemistry and Clinical Biochemistry Catholic University School of Medicine Rome Italy
出 版 物：《Advances in Alzheimer's Disease》 (阿尔茨海默氏病研究进展（英文）)
年 卷 期：2013年第2卷第3期
页 面：99-108页
学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
主 题：S100b Neurodegeneration Oxidate Methionine Apoptotic Genes Expression
摘 要：Amyloid beta (1-42) peptide is considered responsible for the formation of senile plaques that accumulate in the brain of patients with Alzheimer’s disease (AD). In the past years considerable attention has been focused on identifying new protective substances that prevent or almost retard the appearance of amyloid beta (1-42)-related neurotoxic effects. In this study, human neuroblastoma cells (IMR-32) was used as system model to evaluate the protective role of S100b, a neurotrophic factor and neuronal survival protein, that is highly expressed by reactive astrocytes in close vicinity of beta-amyloid deposits, against amyloid beta (1-42)-dependent toxicity. Our results show that at nanomolar concentrations, S100b protects cells against Aβmediated cytotoxicity, as assessed by MTS vitality test. The protective mechanism seems to be related to the effect on bcl-2 (an anti-apoptotic gene) expression, which is highly down-regulated by amyloid beta (1-42) treatment, while resulted more expressed in the presence of S100b. On the contrary, Bax, a proapoptotic gene, resulted down-regulated by the treatment with S100 compared with the results obtained in the presence of amyloid beta (1-42) peptide. However, at micromolar doses, S100b is toxic for IMR-32 cells and its toxicity adds to that of the Aβpeptide, suggesting that additional molecular mechanisms may be involved in theneurotoxic process.
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